Portland Cement Dust 

Hazard assessment document 

EH75/7 
FOREWORD 

This Hazard Assessment Document has been published by the UK Health 

and Safety Executive (HSE). It is aimed at a technical audience and reports 

on the scientific information which underpins the hazard assessment of a 

specific substance. 

In Great Britain, substances which cause harm to health are subject to the 

Control of Substances Hazardous to Health Regulations (COSHH) 2002 (as 

amended). The Regulations require employers to prevent or, if that is not 

reasonably practicable, adequately control employees’ exposure to hazardous 

substances. 

Hazard Assessment Documents are produced to facilitate the development of 

HSE’s regulatory position on a specific health-related issue, which may relate 

to an individual hazardous substance, or may involve consideration of more 

general issues related to chemicals and ill health. The documents in this 

series cover issues relating only to toxicological hazards; other document 

series address issues which involve consideration of occupational exposure 

and risk: 

• Exposure Assessment Document – EH74 series; 

• Risk Assessment Document – EH72 series. 

The data in Hazard Assessment Documents are assessed and endorsed by 

the Working Group on the Assessment of Toxic Chemicals (WATCH). 

WATCH makes recommendations to the Advisory Committee on Toxic 

Substances (ACTS) on all aspects of chemical hazard and risk assessment 

and risk management issues, including recommendations for occupational 

exposure limits (OELs) and other aspects of occupational health risk 

management, as part of its assessment of the substance under discussion. 

Hazard Assessment Documents are published after their endorsement by 

WATCH. 

3 
Contents Page 

1. Summary 6 

2. Introduction 7 

3. The Health Effects Literature 9 

3.1 Effects of single exposure 9 

3.2 Irritation 10

 3.3 Skin sensitisation 10 

3.4 Effects of repeated exposure to cement dust 12 

3.4.1 Recent studies of non-malignant respiratory 12 

disease in workers with long-term exposure to 

cement dust 

3.4.2 Mortality and cancer studies involving workers 28 

with long-term exposure to cement dust

4. References 46

Table 1 Summary of recent studies of non-malignant respiratory 51 

disease in workers with long-term exposure to cement dust 

Table 2 Summary of mortality and cancer morbidity studies in 52 

cement manufacturing workers or masons 

Table 3 Summary of German case control studies for cancers 53 

of the oral cavity, pharynx and larynx
CI 

GLOSSARY 

ATS American Thoracic Society 

Confidence interval 

COPD Chronic obstructive lung disease 

FEF Forced expiratory flow 

FEV1 Forced expiratory volume in one second 

FVC Forced vital capacity 

MRC Medical Research Council (UK) 

MVV Maximum voluntary ventilation 

OR Odds ratio 

PEFR Peak expiratory flow rate 

RR Relative risk 

SD Standard deviation of the mean 

SE Standard error of the mean 

SIR Standardised incidence ratio 

SMR Standardised mortality ratio 

TWA Time weighted average 

VC Vital capacity 

WHO World Health Organization 

5 
1. SUMMARY 

This hazard assessment updates the health effects sections of an earlier HSE 

review of Portland cement (HSE 1994). The latter is taken to represent an 

accurate assessment of the literature available up to 1991. This assessment 

concentrates on the evidence for non-malignant respiratory disease and 

carcinogenicity. The primary literature on skin sensitisation has not been 

reviewed because the potential for cement to cause such reactions, due to the 

presence of hexavalent chromium, has been established by other reviews. 

Toxicological endpoints such as reproductive toxicity and mutagenicity have 

not been considered because there are no data. 

Concerning non-malignant respiratory disease, HSE (1994) noted evidence 

that repeated exposure to Portland cement has produced chronic bronchitis 

and impaired pulmonary function, but firm conclusions could not be drawn 

because of limitations of the available studies. The effects of long-term 

exposure remain poorly studied, particularly because there are no longitudinal 

prospective studies in workers exposed to cement. However, many of the 15 

recent studies, all conducted outside of the UK, provide evidence of the 

presence of respiratory problems among cement factory workers, consistent 

with the earlier literature. Overall, the pattern of evidence clearly indicates that 

occupational exposure to cement dust has produced deficits in respiratory 

function. However, the evidence available at the present time is insufficient to 

establish with any confidence the dose-response relationship for these effects. 

HSE (1994) concluded that there was no convincing evidence for an 

increased incidence of any site-specific cancer resulting from cement 

exposure, but acknowledged that the data available at that time were not 

consistently and reassuringly negative. Since the early 1990s, a number of 

relevant cancer cohort and case control studies have been published, 

conducted in groups exposed to cement either through employment in cement 

factories or in the construction industry. Among these and earlier studies, 

increased incidences of cancers at several sites (stomach, lungs, colon, 

pharynx and larynx) were noted, but taking account of limitations in the 

strength of the observed associations, it is concluded that a causal 

association between Portland cement exposure and cancer has not been 

established. Nevertheless, the findings of the recent studies reviewed in this 

document maintain the uncertainty concerning a possible risk of cancer raised 

by the earlier data reviewed by HSE (1994). 

6 
2. INTRODUCTION 

This hazard assessment document updates the health effects sections of an 

earlier HSE review of Portland cement (HSE 1994). The latter is taken to 

represent an accurate assessment of the literature available up to 1991. 

Consequently this hazard assessment concentrates mainly on literature 

published after this time, although certain pre-1991 studies are considered in 

some detail where they help with the interpretation of the recent literature. A 

copy of the earlier HSE (1994) review is provided as Annex 2 to the 

WATCH/2005/03. 

There were two reasons for producing this updating document. Firstly, workrelated chronic obstructive pulmonary disease (COPD) is a priority within 

HSE’s Occupational Respiratory Disease (ORD) sub-programme. The 

evidence-base for this sub-programme indicates that occupational exposure 

to dusts in general leads to an increased risk of COPD. Cement dust is a 

particularly alkaline and irritant dust, and might therefore be considered to 

pose a greater risk of respiratory tract damage than many other poorly soluble 

dusts (generically often referred to as “low toxicity dusts”). The HSE (1994) 

review described evidence for an increased risk of chronic bronchitis and 

impairment of pulmonary function (consistent with COPD) in cement dust 

exposed workers, but there was a lack of data on dose-response 

relationships. Hence, one reason for undertaking this updating assessment 

was to see whether the scientific literature on cement dust published over the 

last 10 years is now better able to characterise the risks of COPD, and 

consequently to help determine whether or not cement dust should be 

regarded as a particular priority for action within HSE’s ORD sub-programme. 

In addition, it has been drawn to the attention of HSE that in recent years a 

number of case-control studies have been published suggesting that exposure 

to cement dust may be a cause of laryngeal and pharyngeal cancer. It was felt 

important to examine the evidence from these studies particularly as the 

earlier HSE review of Portland cement (HSE 1994) noted that the evidence for 

carcinogenicity with cement dust was not reassuringly negative, albeit largely 

based on concerns for stomach cancer. Given the widespread occupational 

exposure to cement dust, it was felt important that HSE develop an updated 

position in relation to carcinogenicity. 

Annex 1 provides a detailed explanation of the composition and manufacture 

of Portland cement. In brief, Portland cement is produced by crushing and 

grinding calcareous materials (e.g. limestone, chalk) and argillaceous 

materials (e.g. clay, shale), as a wet slurry or in a dry state. The mixture is 

calcined in a rotary kiln and the resulting clinker is finely ground. The product 

is composed largely of calcium silicates, aluminates, and alumino-ferrites. 

Other constituents are then added, depending on the desired concrete 

properties. 

Hexavalent chromium (Cr (VI)) can be present in cement. The sources of 

chromium are in the raw materials, refractory bricks in the kiln and chromium 

7 
steel grinders. Because of concerns about Cr (VI) sensitisation (see section 

2.3), during recent years several countries have introduced measures to limit 

the amount of Cr (VI) in cement products. This can be achieved by the 

addition of ferrous sulphate to cement, which transforms Cr (VI) to form Cr (III) 

compounds. In 2003 the European Commission introduced new legislation to 

restrict the marketing and use throughout the EU of cement products 

containing soluble Cr (VI) at a concentration of more than 2 ppm. 

This document focuses mainly on the evidence for non-malignant respiratory 

disease and carcinogenicity. Studies published between 1990 and 2004 were 

identified from a literature search using TOXLINE and PubMed, or from report 

reference lists. All relevant reports have been critically appraised. The primary 

literature on skin sensitisation was not reviewed because the hazardous 

properties of cement in relation to this adverse health effect had been 

established in the pre-1991 literature, and the primary literature has been the 

subject of two very recent critical reviews (summarised in section 3.3). Other 

toxicological endpoints such as reproductive toxicity and mutagenicity have 

not been considered. 

Information on the adverse health effects of cement dust comes from 

observations of its effects in humans. As noted in the earlier HSE (1994) 

review, animal data are extremely limited in terms of their scope and quality 

and do not provide any useful information. 

A number of the available epidemiology studies were conducted in Portland 

cement production plant workers. It is noted that these workers can be 

exposed to the raw materials of cement production, which include limestone, 

chalk, clay and shale, to clinker, as well as to Portland cement dust. The exact 

nature of the dust exposures experienced by cement plant workers has not 

been characterised in any of the studies. Consequently, one cannot exclude 

the possibility that any observed adverse health may have been due, at least 

in part, to the raw materials and intermediates of cement production. 

Among the available epidemiological studies, dust exposures have been 

expressed either in terms of respirable dust, or “total dust”, or both. This 

raises two issues, one concerning the ratio between total and respirable dust 

(given that cement dust is very fine and one might expect a high proportion of 

the total dust to be respirable), and the other concerning the meaning of “total” 

dust. In the study of Noor et al. (2000), the ratio of total to respirable dust was 

reported as 8.5 mg.m-3 to 5.7 mg.m-3. In contrast, in the study of Fell et al., the 

ratio of total to respirable dust was 7.4 mg.m-3 to 0.9 mg.m-3. The differences 

in these ratios may be a consequence of measuring dust at different stages of 

the manufacturing process. One might expect a higher proportion of respirable 

dust at the later stages of the manufacturing process as opposed to the earlier 

stages where the raw materials are handled. 

It should be noted that the metrics “total” and “total inhalable” dust are not 

equivalent. In many countries, “total dust” is measured using the NIOSH 

method that involves a 37 mm closed face cassette. This is known to under 

sample for “inhalable dust” as measured using the IOM sampler (25 mm 

forward facing cassette). Although not generally specified, it is likely that the 

8 
“total” dust levels reported in the studies on cement dust refer to 

measurements taken with the NIOSH method, and the results will not be 

equivalent to the UK “total inhalable dust” metric. Overall therefore, the 

exposure data reported in the following studies need to be interpreted with 

care. 

3. THE HEALTH EFFECTS LITERATURE 

3.1 Effects of single exposure 

HSE (1994) reported that there were no data on the effects of a single 

exposure to cement by relevant routes of exposure. 

Only one recent study looking at short-term effects of cement exposure was 

identified. Changes in pulmonary function during a work shift were 

investigated in workers at three Portland cement factories in Saudi Arabia (Ali 

et al. 1998). From the payrolls, 150 exposed male workers were selected 

randomly for the study, in a manner that ensured that all production areas 

were represented. Their mean age (± SE) was 38.0 ± 0.8 years. As an 

unexposed control group, 355 male workers were randomly chosen from 

among administrative staff in the cement, ammonia, petrochemical and 

asbestos industries. The control group was slightly younger, with a mean age 

of 34.3 ± 0.5, and their ethnicity was Arab (68%), Indian subcontinent (22%) 

and South East Asia (9%). Personal information was collected by 

questionnaire. The proportion of current smokers, ex-smokers and nonsmokers was similar in the control and exposed groups. Respirable dust was 

measured using a gravimetric method for a total of 97 samples collected from 

various production areas; the report does not state the sampling time or 

whether these were personal or static samples. Spirometry was conduced 

immediately before and after the morning shift. The highest values from three 

acceptable expirations for FEV1, FVC and FEF25-75% were recorded and the 

FEV1/FVC ratio was calculated. 

The geometric mean concentration (± SD) of respirable dust ranged from 20 ± 

1 mg.m-3 in the quarry to 7 ± 2 mg.m-3 in the kiln area. Spirometry data were 

reported as mean cross-shift changes. The spirometry readings did not 

appear to have been adjusted for height. Reductions in FEV1, FEV1/FVC ratio 

and FEF25-75% occurring during the workshift were significantly greater in the 

exposed workers. For example, the mean (± SE) reduction in FEV1 was 0.022 

± 0.008 l for the control group, compared with 0.077 ± 0.011 l for the exposed 

group. For FEV1/FVC the mean reduction was 0.011 ± 0.165% and 1.316 ± 

0.319% for the control and exposed group. Regression analysis demonstrated 

no relationship between cross-shift pulmonary changes and age or smoking 

status. 

The results of this study suggest that bronchoconstriction had occurred during 

the workshift for the cement workers, who were exposed to relatively high dust 

concentrations. The health significance of this effect is uncertain. 

9 
3.2 Irritation 

HSE (1994) concluded that cement has irritant and corrosive properties, 

especially when wet, towards the skin. Also, it was concluded that due to its 

alkalinity, moistened cement would also produce eye irritation. 

As these properties of cement are well established, no further evaluation of 

the literature has been conducted for these adverse health effects in the 

present review. 

Portland cement is generally considered to be a respiratory tract irritant, 

although there are no data on this aspect in the scientific literature. 

3.3 Sensitisation 

HSE (1994) stated, based on a review of the pre-1979 literature (Fleetwood 

and Soutar 1979), ‘that there have been many cases of cement dermatitis 

appearing to arise as a result of skin sensitisation to hexavalent chromium 

(Cr(VI)) in cement’. Concerns for sensitisation relate in the main to contact 

with the wet cement. 

Recently the National Institute of Occupational Health, Norway (NIOH, 2003) 

conducted a detailed critical review of the literature, to address these 

questions: 

1. Does Cr(VI) in wet cement cause allergic dermatitis (skin 

sensitisation) in construction workers? 

2. Is there any causal association between the reduction of Cr(VI) in 

cement and the occurrence of allergic dermatitis? 

Twenty four papers published between 1975 and 2001 were systematically 

reviewed. These were selected as studies of chromate allergy in humans, 

especially those involving construction workers, which included the conduct of 

patch tests for chromate allergy. Most of the investigations were crosssectional studies based on patients attending dermatology clinics, in the 

general population, or in groups of construction workers. Some studies 

provided limited comparative information on the prevalence of Cr(VI) 

sensitisation in groups of workers exposed to cement with ‘high’ and ‘low’ 

(less than 2 ppm) Cr(VI) content, conducted in countries where the practice of 

reducing the Cr(VI) content of cement by the addition of ferrous sulphate has 

been introduced. 

All the studies reviewed were considered by NIOH to have significant 

limitations, notably the absence of exposure characterisation, problems with 

the chromate allergy diagnosis, subject selection bias and the lack of 

prospective follow-up. Nevertheless, the reviewers identified a consistently 

high prevalence of Cr(VI) allergy in studies of construction workers. Also, in 

general population studies, the prevalence of allergy was found to be higher in 

construction workers than in other occupational groups. Furthermore, 

analyses of patients attending dermatology clinics with a diagnosis of 

chromate allergy revealed a high proportion of patients with occupations 

involving contact with cement. 

10 
In view of the consistency and strength of the associations it was concluded 

that, despite their limitations, the available studies supported the hypothesis of 

a causal relationship between Cr(VI) in wet cement and allergic contact 

dermatitis in construction workers. 

In answer to the second question, it was concluded that there is insufficient 

information to decide if there is a causal association between the reduction of 

Cr(VI) in cement and a reduced occurrence of allergic dermatitis. However, 

the information that is currently available supports such a relationship. 

Furthermore, it is biologically plausible that that a reduction in exposure to 

Cr(VI) will lead to a lower risk of allergic contact dermatitis. 

Recently the European Commission’s Scientific Committee on Toxicology, 

Ecotoxicology and the Environment (SCTEE, now the Scientific Committee on 

Health and Environmental Risks) expressed an opinion of the risks to health 

from Cr(VI) in cement (European Commission, 2002). On the basis of a 

selective review of the published literature, SCTEE concluded that Cr(VI) 

compounds in cement induce sensitisation and cause serious allergic 

reactions in construction workers. Also they concluded that water-soluble 

Cr(VI) compounds penetrate the skin to a much greater extent than the less 

water-soluble Cr (III) compounds, and that Cr(VI) readily penetrates wet 

leather gloves. SCTEE also concluded that, based on studies in Denmark 

(Avenstorp, 1989a,b, 1991, 1992), a reduction of Cr(VI) compounds in cement 

to less than 2 ppm will reduce the prevalence of allergic cement eczema in 

workers, and will reduce the risk of becoming sensitised to chromate. They 

also emphasised that education and the use of personal protective measures 

would also contribute to a lower frequency of skin sensitisation due to Cr(VI). 

Subsequently the European Commission introduced new legislation, through 

an amendment (2003/53/EC) to the Marketing and Use Directive 

(76/769/EEC), to restrict the marketing and use of cement and cement 

containing preparations where the level of soluble Cr(VI) is more than 2 ppm. 

Overall, it can be concluded that contact with wet cement can cause 

sensitisation reactions to Cr(VI) in the cement and, though not proven, is likely 

that reducing the Cr(VI) content of cement will reduce the risks of Cr(VI) 

sensitisation reactions in workers who have contact with cement. 

11 
3.4 Effects of repeated exposure to cement dust 

3.4.1 Recent studies of non-malignant respiratory disease in workers 

with long-term exposure to cement dust 

HSE (1994) noted evidence that repeated exposure of humans to Portland 

cement has produced rhinitis, chronic productive cough (chronic bronchitis), 

slight abnormalities on chest radiography and impaired pulmonary function. 

However, it was considered that the quality of studies indicating adverse 

effects on pulmonary function was such that the evidence for a true effect of 

cement dust is inconclusive. From the limited exposure data available, and 

from subjective descriptions of working conditions, the respiratory effects 

appeared to be associated with very dusty working conditions. Although no 

firm conclusion could be drawn about the dose-response relationship for the 

respiratory effects, attention was drawn to several studies which reported no 

significant effects associated with airborne concentrations of cement dust of 

2.9 mg.m-3 total dust and 0.57 mg.m-3 respirable dust (geometric means), up 

to 5 mg.m-3 total dust and 1.1 mg.m-3 respirable dust, or 2-7.8 mg.m-3 total 

dust and 1-2.2 mg.m-3 respirable dust. 

The literature search conducted in 2004 identified a number of recently 

published cross sectional studies, together with one retrospective cohort 

study, of non-malignant respiratory disease conducted in workers at cement 

production plants. In 11 studies, pulmonary function testing was conducted 

and information on the presence of self-reported respiratory symptoms was 

usually collected. Pulmonary function testing was by spirometry, except for 

one study that used a peak flow meter. One cross sectional study investigated 

workers using chest radiography. A further 3 studies in cement production 

workers looked only at self reported respiratory symptoms. All these 15 

studies are appraised below, and summarised in Table 1. 

Two general health surveys of populations of construction workers are 

available (Petersen and Zelling 1998 and Arndt et al. 1996) but these studies 

do not provide any information on health that can be related to cement dust 

exposure so these studies were not included in this review. 

3.4.1.1 Retrospective cohort study, which included pulmonary function testing 

Fell et al. (2003) conducted a retrospective cohort study in 119 Norwegian cement 

factory workers. A respiratory questionnaire was administered and spirometry was 

conducted. Current dust level measurements were available and a semi-quantitative 

cumulative exposure matrix was developed. The study showed no differences in the 

respiratory health of the cement workers exposed to average respirable dust levels of 

at least 1 mg.m-3 when compared with matched blue-collar controls 

In a recent retrospective cohort study, pulmonary function and the presence of 

respiratory symptoms were investigated in a group of Norwegian Portland 

cement factory workers (Fell et al. 2003). The investigation was conducted in 

1998 and 1999. The study population comprised men born between 1918 and 

1938 who had worked at a particular cement-producing factory for at least one 

year; presumably most of the study population were retired. A total of 226 

12 
workers fulfilling these criteria were identified, of which 148 were still alive. No 

information was available on the cause of death of those who had died. After 

exclusions due to white collar work, workplace exposures to paint or welding 

fume, medical conditions unrelated to work that would affect ability to undergo 

spirometry testing, refusal to participate or not being contactable, 119 workers 

were available for the study. Only 4 workers refused to participate. They had a 

mean age of 69 years, and a mean of 21.8 years exposure to cement dust. As 

controls, a group of 94 men born between 1918 and 1938 and who had 

worked at an ammonia plant for at least one year were identified; 63 were still 

alive at the time of the study. The ammonia plant was located about 10 km 

from the cement plant. It used closed processes, so the workers were not 

exposed to ammonia. None of the control workers had ever experienced 

exposure to ammonia at levels sufficient to cause symptoms of sensory 

irritation. After exclusions due to refusal to participate or not being 

contactable, 50 controls, of mean age 67 years were available for 

investigation. The percentage of deceased workers in the cement workers and 

controls was similar, at about 35%. The proportion of current smokers was 

slightly higher among the cement workers (35%) than the controls (26%). 

Previous dust exposures for particular work processes were estimated from 

documented information on changes in work practice and from detailed 

interviews with a subgroup of workers. Four levels of historical exposure were 

established, and assigned semiquantitative exposure numbers. Cumulative 

exposure indices were calculated for each worker for an exposure-response 

analysis. Contemporary dust exposure was measured by personal sampling, 

over 8 hour periods on three days of work; 20 person-related measurements 

were conducted. Silica levels were measured in the three samples showing 

the highest amounts of dust. Information on respiratory symptoms was 

gathered, using a Norwegian modification of the MRC questionnaire, 

answered at home. Also, information on job history, cement dust exposure 

level estimates, asbestos exposure and smoking habits were gathered. 

Spirometry was conducted in accordance with ATS guidelines by an 

investigator who was only ‘partially’ blinded to exposure status. A diagnosis of 

COPD was made in subjects with a history of chronic cough, phlegm when 

coughing, breathlessness and/or wheezing and also with FEV1/FVC ratio of 

less than 70%. 

In the contemporary workplace air samples the mean concentration for total 

dust was 7.4 mg.m-3 (range 0.4 - 53.7 mg.m-3) and for respirable dust 0.91 

mg.m-3 (all respirable dust measurements were below the Norwegian 

exposure limit of 5 mg.m-3). Silica was not detected in two samples and was 

0.06 mg.m-3 in the third sample, below the local limit. The prevalence of 

respiratory symptoms was slightly higher in the cement workers, and 

positively associated with cumulative exposure index for three of the 

symptoms; however, there were no statistically significant differences between 

the control and exposed workers. There were no significant differences for the 

spirometry parameters, after adjustment for age, height, tobacco use and 

asbestos exposure. For the controls and exposed workers, FVC was 86 and 

89% of predicted (according to age, height and gender), FEV1 was 85 and 

90% of predicted and FEV1/FVC ratio was 73 and 74%, respectively. Among 

13 
the cement workers the spirometry results were similar for the workers within 

the highest and lowest cumulative exposure quartiles. The prevalence of 

COPD was 14% for controls and 14.3% for exposed workers. 

Overall, this study showed no differences in the respiratory health of surviving 

workers exposed to cement plant dust and a comparable group of nonexposed workers. This study included an assessment of workers who had left 

the cement plant, so the potential for selection bias due to the exclusion of 

individuals who may have left the cement plant because of work related illhealth was reduced. However, no information on the causes of death among 

the 35% of workers who were deceased was available so the possibility of 

selection bias resulting from the exclusion of individuals who died of 

respiratory disease cannot be excluded. Nevertheless, the percentage of 

deaths in the two groups was similar suggesting that if selection bias was 

present it was minimal. A weakness of the semi-quantitative dose-response 

assessment is that this relied on estimates of cumulative exposure in the 

absence of historical dust measurement. Inaccuracies in the exposure 

estimation would result in a tendency for the masking any exposure-response 

relationship, if present. 

One limitation of this study is that it is not possible to draw firm conclusions 

about the maximum airborne concentration of cement plant dust that would 

not be associated with adverse respiratory health because of the absence 

historical quantitative exposure measurements. Nevertheless, if it is assumed 

that historical exposures were at least as high as contemporary exposures, 

the study provides reassurance that the control of cement dust levels to 

around 1 mg.m-3 (respirable dust) will provide protection against adverse 

effects on respiratory health. 

3.4.1.2 Cross sectional studies which included pulmonary testing 

Mwaiselage et al. (2004) studied 115 Tanzanian cement factory workers. Pulmonary 

function was investigated by spirometry and peak flow measurement. Current total 

dust exposure measurements were available, from which cumulative exposures were 

estimated. Lung function was poorer in the occupational goups with current mean dust 

exposure of 3.2 mg.m-3 and above (cumulative dust exposure 36 mg.m-3year and 

above).. The risk of developing a notable obstructive impairment, represented by a 

FEV1/FVC ratio <0.7, was significantly increased for cumulative dust exposures in 

excess of 300 mg.m-3year. 

In a recent study, pulmonary function was investigated in male workers at 

Tanzanian Portland cement factory (Mwaiselage et al. 2004). The exposed 

study population was all 126 production workers at the plant. A control group 

was made up of all 88 maintenance workers and 32 randomly selected 

administrative workers. After exclusions because of refusal to participate 

(about 4%), unsatisfactory spirometry performance, physician diagnosed 

asthma or the presence of other diseases that could affect pulmonary 

function, 115 exposed subjects and 102 controls were available for the final 

analysis. The mean duration of employment for the exposed group was 12 

years and for the controls 15 years. Information on personal characteristics, 

smoking, use of personal protective equipment and occupational history were 

14 
obtained by standardised questionnaire. Spirometry was conducted during the 

morning, and to ATS guidelines. PEFR was measured by Vitalograph peak 

flow meter. FEV1, FVC and PEFR were expressed as absolute values and as 

% of predicted with reference to age and height adjusted values for the male 

Tanzanian population. A person was considered to have airflow limitation if 

the FEV1/FVC ratio was <0.7. A contemporary dust exposure assessment 

was based on 120 full-shift personal samples of total dust, collected from 52 

exposed and 28 control subjects. Dust exposures were also expressed for 

each occupational group as a cumulative mean, calculated as the product of 

the geometric mean concentration and the number of years worked in the 

particular group. 

Smoking was more prevalent in the exposed group, with 32% being eversmokers, compared with 25% among controls. Mean cumulative total dust 

exposure was 11 mg.m-3year (range 0.3-38) for the controls and 69 mg.m-3 

year (range 3-926) for the exposed group. Approximately 30% of production 

and maintenance works reported wearing disposable protective face masks 

regularly, although the quality and effectiveness of these masks could not be 

determined. The report stated that there was no correlation between face 

mask use and lung function, but no data were presented. 

A summary of the dust exposure and lung function data is presented in 

following table. FEV1% and FEV1/FVC ratio was much lower and the 

prevalence of airways obstruction was higher in the occupational goups with 

current mean dust exposure of 3.2 mg.m-3 and above (cumulative 36 mg.m-3 

and above). 

Admin Mainten Raw mill Kiln Cement Crusher Packing Crane 

(n=19) -ance (n=17) (n=26) mill (n=18) (n=30) (n=13) 

(n=83) (n=11) 

Mean current 0.3 1 1.8 2.9 3.2 13.5 21.3 38.6 

total dust (0-2) (0-10) (1-4) (1-10) (1-8) (0-63) (23-230) (8-140) 

exposure 

mg.m-1 (range) 

Mean 4 14 21 12 36 158 230 378 

cumulative total (0-10) (1-38) (9-43) (3-87) (22-74) (41-405) (43-639) (77-926) 

dust exposure 

mg.m-1 (range) 

Smoking (pack 3.4 2.4 1.7 0.9 3.0 3.2 1.9 1.4 

years) 

FEV1 % 97 ± 15 100 ± 12 96 ± 16 91 ± 10 77 ± 8 79 ± 14 74 ± 14 78 ± 12 

predicted (±SD) 

FEV1/FVC 0.86 ± 0.87 ± 0.90 ± 0.81 ± 0.75 ± 0.74 ± 0.72 ± 0.72 ± 

(±SD) 0.12 0.07 0.1 0.06 0.0.05 0.09 0.10 0.06 

Number with 1 (5%) 5 (6%) 1 (7%) 1 (4%) 2 (18%) 5 (28%) 14 (47%) 3 (23%) 

airflow limitation 

(%) 

A statistical comparison of the results for all exposed workers were compared 

with the maintenance/administrative controls. Percentage predicted FEV1 for 

the exposed group (mean ± SD, 82% ± 15) was lower than for controls (99% ± 

15 
12). Similarly, FEV1/FVC for the exposed group (0.77 ± 0.1) was lower than 

for controls (0.87 ± 0.1), as was PEFR (80% ± 5 vs. 88% ± 7). These 

differences were statistically significant. Similar differences were observed for 

comparisons between ever smokers of the exposed and control groups (after 

adjusting for number of packs smoked) and never smokers of the exposed 

and control groups. Linear regression analysis, taking account of height, age 

and smoking, showed a negative correlation between cumulative dust 

exposure and the following lung function parameters: FEV1, FVC, FEV1/FVC 

ratio and PEF. 

. The OR relating to FEV1/FVC ratio <0.7 for occupational groups in the 

cumulative exposure band 100-300 mg.m-3 year was 1.6 (95% CI 0.5-5.1) and 

for >300 mg.m-3 year was 9.9 (95% CI 3.5-27.8), after adjustment for age and 

smoking. 

To conclude, this study demonstrated reduced lung function in cement 

production workers in comparison with a control group with relatively low dust 

exposure. A strength of this study is that a meaningful analysis for doseresponse relationships was possible because subgroups with very contrasting 

dust exposure levels were identified. This analysis demonstrated that lung 

function was poorer in the occupational goups with current mean dust 

exposure of 3.2 mg.m-3 and above (cumulative dust exposure 36 mg.m-3year 

and above). and that the risk of developing a notable obstructive impairment 

(i.e. represented by a FEV1/FVC ratio <0.7) was significantly increased for 

cumulative total dust exposures in excess of 300 mg.m-3 year. A weakness of 

this study is that only contemporary exposure data were available and so the 

reliability of the cumulative exposure estimates is uncertain. The authors 

stated that conditions at the factory and production capacity had changed little 

since opening in 1965, and they considered it was reasonable to assume that 

dust exposure levels had remained constant, but questions still remain. The 

report did not mention whether workers changed jobs within the factory; if this 

did occur, then exposure group misclassification is possible, which would 

have the effect of masking a dose response relationship. Overall, this study 

provided evidence of an association between reduced lung function and 

current total dust exposures in excess of 3 mg.m-3 and an obstructive 

impairment associated with cumulative cement exposures likely to be in 

excess 300 mg.m-3year. 

Laraqui Hossini et al. (2002) investigated the respiratory health of 280 Moroccan 

cement factory workers by respiratory questionnaire and spirometry. No dust exposure 

measurements were taken, but levels were described as being relatively high. There 

was a higher prevalence of respiratory symptoms and minor spirometry deficits among 

the cement workers, compared with controls. 

Pulmonary function and the presence of respiratory symptoms were 

investigated in workers at a Moroccan cement factory (Laraqui Hossini et al. 

2002). The study population was 280 workers exposed to cement dust, of 

mean (± SD) age 41 ± 6 years and duration of employment 14 ± 4 years. As a 

control group, 73 non-exposed administrative workers from the same factory 

were recruited, of mean age and duration of employment of 37 ± 7 and 13 ± 4 

years, respectively. Recruitment methods were not described. All exposed 

and control subjects had been employed at the factory for at least 2 years, 

16 
and none were found with respiratory or cardiac symptoms at a preemployment medical examination. The proportion of current, ex- and nonsmokers in the two groups was similar. Demographic information and medical 

histories were obtained using a standardised questionnaire based on those of 

the MRC and WHO. Chronic bronchitis was defined as productive cough for 

at least 3 months of the year, for at least 2 years. Respiratory function was 

assessed by spirometry, using standard methods. The highest values from 

three expirations for FVC and FEV1 were recorded and FEV1/FVC ratio was 

calculated. Workers with deficits were graded as having an ‘alveolar’, slight 

(FEV1 71-80% of predicted), moderate (FEV1 61-70% of predicted), serious 

(FEV1 41-60% of predicted) or severe (FEV1 below 40% of predicted) deficit 

according to an official French government grading system. Cement plant dust 

exposure for the exposed group was graded in a semi-quantitative manner as 

low, moderate and high, depending on the job within the plant. 

Dust concentration in the workplace was not measured, but in the crushing 

shop, production plant and packing areas the concentration was such that 

vision was impeded and dust was deposited on hair and clothing. The 

prevalence of respiratory symptoms was higher among the exposed workers, 

with 65% reporting symptoms compared with 35% of controls. Most common 

symptoms were coughing, phlegm, dyspnoea and rhinitis. Approximately 30% 

of exposed workers were considered to have chronic bronchitis compared to 

10% of controls, with the prevalence being greatest for workers with the 

highest dust exposure, those employed for more than 10 years, and among 

current and ex-smokers. Abnormal spirometry results were found in 22% of 

exposed workers compared with 14% of controls, although most (78%) 

abnormalities were graded as an ‘alveolar’ or slight deficit. There was no clear 

relationship between the level of exposure and spirometry results. 

This study shows an increased prevalence of respiratory symptoms and 

deficits in spirometry in cement exposed workers in comparison with the 

control group. A key weakness of this study is the lack of quantitative 

exposure data. Also, the cement dust exposed group were compared to 

administrative workers, who may have a different respiratory health status 

irrespective of the influence of cement exposure. 

Meo et al. (2002) conducted spirometry in 50 Pakistani cement mill workers. No 

information on dust exposure levels was available. FVC and FEV1 were reduced and 

FEV1/FVC ratio was increased for the cement workers, in comparison with matched 

controls. 

Pulmonary function was investigated in a group of 50 male workers from a 

Karachi cement mill (Meo et al. 2002). The study subjects were volunteers, 

selected at random. They were described as apparently healthy, aged 20 - 60 

years (mean 36.9), and had been exposed to cement dust for a mean of 13 

years. The control group comprised 50 healthy males, selected from the local 

Karachi population. They were matched with the exposed group for age, 

height, weight and socio-economic status. Subjects with a range of medical 

conditions or who smoked or abused drugs were not included in the study. 

17 
Spirometry was conducted in accordance with ATS guidelines. The highest 

values from three expirations of the following parameters were recorded: FVC, 

FEV1, FEV1/FCV ratio, PEF and FEF25-75% and MVV. 

Mean FVC and FEV1 were significantly reduced in the group of cement 

workers. For the controls and cement workers FVC (mean ± SE) was 4.03 ± 

0.09 and 3.18 ± 0.11 litres and FEV1 was 3.04 ± 0.08 and 2.54 ± 0.10 litres, 

respectively. FEV1/FCV ratio was significantly increased for the cement 

workers; the ratios were 75.8 ± 1.4 and 81.5 ± 2.3% in controls and cement 

workers, respectively. PEF and MVV were significantly lower in the cement 

workers, but FEF25-75% was similar to the controls. 

The reductions in FVC and FEV1 accompanied by an increase in FEV1/FVC 

ratio seen in the cement workers are consistent with the presence of a 

restrictive impairment of lung function. Overall, this study suggests that longterm exposure to cement dust can cause an impaired respiratory function, 

consistent with the previous study. However, a limitation of this study is that 

the exposed and control subject selection procedures were not adequately 

described, so it is not possible to judge if selection bias was introduced. 

Another limitation of the study is that there is no information on dust exposure, 

or a description of the working conditions at the cement mill so it is not 

possible to relate the lung function differences to dust exposure levels in a 

quantitative manner. 

Al-Naomi et al. (2001) investigated the respiratory health of 75 cement factory workers 

in the United Arab Emirates by respiratory questionnaire and spirometry. No 

information on cement dust exposure levels was available. Among the cement workers 

there was a higher prevalence of respiratory symptoms and a reduction in spirometry 

measurements, in comparison with matched controls. 

Pulmonary function and the presence of respiratory symptoms were 

investigated in a group of workers of Pakistani or Bangladeshi origin at a 

United Arab Emirates cement-producing factory (Al-Naomi et al. 2001). All 75 

workers at the factory were invited to participate. Eight workers did not 

participate, either because they were on leave at the time of the study, or 

were senior management personnel. None reported a history of allergic or 

chronic respiratory disease prior to joining the cement industry. A control 

group was selected as a group of similar age, nationality and socio-economic 

status, and with no history of chronic respiratory disease or history of 

occupational exposure to dust chemicals fumes or gases. They were selected 

from those seeking a certificate of good health from a medical clinic so that 

they could renew their residency permit; the report described them as ‘retail 

salesmen’. Of the136 unexposed workers invited to participate, 134 accepted. 

Information on general and respiratory heath and lifestyle was collected using 

an interviewer-administered modification of the MRC standardised 

questionnaire on respiratory symptoms. It was not stated if the interviewer 

was blinded to exposure status. Also, information on the use of personal 

protective equipment was collected. Body mass index (BMI) was calculated 

from height and weight measurements, and blood pressure was measured. 

Smoking was analysed as ‘pack-years’ (smoking 20 cigarettes a day for one 

18 
year was defined as a pack-year). Spirometry was conducted according to 

ATS recommendations. 

The control and exposed groups were similar with respect to age (mean ± SD 

44.4 ± 7.5 and 44.2 ± 9.9 years, respectively, although elsewhere in the report 

the mean age of the control group is given as 32.1 years), BMI, blood 

pressure and education. However, there was a large and statistically 

significant difference in cigarette consumption; pack-years were 0.5 ± 0.05 for 

controls and 4.6 ± 1.1 for the exposed group. The percentage of workers selfreporting the following chronic respiratory symptoms were higher in the 

exposed group: cough (10% in control vs. 30% in exposed group), phlegm 

(5% vs. 25%), wheeze (3% vs. 8%), dyspnoea (5 vs. 21%), sinusitis (11% vs. 

27%). Asthma was higher in the exposed group (3% vs. 6%). Bronchitis, 

defined by the presence of phlegm/cough for at least 3 months of the year, 

was reported in 4% of controls compared with 13% of exposed workers. All 

spirometry parameters were significantly lower in the exposed group. In the 

control and exposed groups, respectively, FVC was (mean ± SE) 3.42 ± 0.05 

and 3.17 ± 0.08 l, FEV1 was 2.99 ± 0.04 and 2.59 ±0.07 l/s, and FEV1/FVC 

ratio was 87.64 ± 0.58 and 81.78 ± 1.11%. Within the group of exposed 

workers, spirometry values were lower among supervisors (13 workers), 

attendants (5) and machine operators (23) who were said to work on the 

factory floor longer than maintenance workers. The percentages of exposed 

workers with a mild impairment of FEV1 (defined as below the lower 95% CI 

for the predicted value but >60% of predicted) were greater than the controls 

(43% in controls vs. 67%). Only one subject in the study, who was in the 

exposed group, had a more severe impairment. A comparison of the 

spirometry results for exposed workers who were smokers and non-smokers 

showed few differences, suggesting the smoking did not have an effect on the 

spirometry results (although the report text described ‘significantly lower 

values’ for smokers which were not apparent in the results table). Overall, this 

study showed a higher prevalence of chronic respiratory symptoms and 

reduced pulmonary function in cement workers, compared with a group of 

workers who were not exposed to dusts and chemicals. However, there are 

inconsistencies in the reporting of the study, and uncertainties regarding the 

role of smoking in the differences observed between the cement workers and 

controls. Consequently the reliance that can be accorded to this study is 

limited. 

Noor et al. (2000) investigated 62 Malaysian cement factory workers. A respiratory 

questionnaire was administered and spirometry was conducted. Current dust 

measurements were available. There was a higher prevalence of respiratory symptoms 

and a reduction of FVC, FEV1 and FEV1/FVC ratio among the cement workers compared 

with controls that were university staff or students. 

In a briefly reported study, pulmonary function and respiratory symptoms were 

investigated in workers at a Malaysian Portland cement-producing factory 

(Noor et al. 2000). Subject selection procedures were not described. Sixty-two 

cement workers were selected for study; 32 were non-smokers with a mean 

age of 35 years and 30 were smokers with mean age of 37. They had worked 

at the factory for between 0.5 and 38 years. Seventy university students and 

staff, all not current smokers with mean age of 37, served as controls. 

19 
Airborne dust levels were determined from 2 hour samples taken at six static 

sampling points in the cement factory and one at the university. Dust was 

fractionated into ‘fine’ (diameter <10 μm) and ’course’ diameter <10 μm 

particles. Spirometry was conducted according to standard methods. Lifestyle 

and medical information were collected using an ATS questionnaire. 

Dust measurements in the cement factory were highest in a packing area, 

with total dust concentrations of 10.2 mg.m-3 of which 8.0 mg.m-3 were fine 

particles. In other areas the total dust concentrations ranged from 3.4 to 0.2 

mg.m-3. FEV1 and FEV1/FVC ratio, unadjusted for height and age, were 

reduced in both non-smoking and smoking cement workers, in comparison 

with the control group. These differences were more marked when the 

analysis was limited to subjects aged 30 – 40. For these subgroups, for 

controls, non-smoking and smoking cement workers, respectively, mean (± 

SE) FEV1 was 3.0 ± 0.1, 2.7 ± 0.1 and 2.7 ± 0.2 l and FEV1/FVC ratio was 

95.5 ± 1.1, 85.4 ± 1.6 and 81.1 ± 3.7%. The differences between the controls 

and both groups of cement workers were statistically significant. The height 

distribution within each of these subgroups was similar. Mean FEV1 when 

expressed as a percentage of predicted (using a Malaysian reference 

population) was reduced in both non-smoking and smoking cement workers 

compared with controls; values for the control and two respective control 

groups were 102 ± 2, 92 ± 4 and 96 ± 4%. The cement workers were stratified 

according to whether they worked in areas with high (mean of 8.5 mg.m-3), 

medium (2.8 mg.m-3) or low (0.58 mg.m-3) dust concentrations and it was 

found the spirometry parameters generally had the lowest mean values in the 

high exposure group. The prevalence of three respiratory symptoms was 

significantly higher among cement workers. These were morning cough (in 

6% of controls vs. 25% of cement workers), morning phlegm (11% vs. 24%) 

and chest tightness (6% vs. 19%). 

Overall, this study showed a higher prevalence of chronic respiratory 

symptoms and reduced pulmonary function in cement workers, compared with 

university students/staff. One weakness of the design of this study is that the 

exposed and control groups were unlikely to be equivalent in terms of socioeconomic status, a possible confounding factor. Nevertheless, among the 

cement workers the effects on pulmonary function were most marked for 

those with the highest dust exposures, suggesting that cement exposure can 

affect respiratory health. 

Mengesha et al. (1998) administered a respiratory questionnaire and conduced 

spirometry and peak flow measurements in 53 Ethiopian cement factory workers. 

Current dust measurements were available. There was a higher prevalence of 

respiratory symptoms among cement workers, compared with controls. FVC, FEV1 and 

FEV1/FVC ratio were lower for the group with the highest dust exposures. 

Pulmonary function and the presence of respiratory symptoms were 

investigated in persons working in dusty environments in Ethiopia (Mengesha 

et al. 1998). Among those investigated were 53 cement factory workers, all 

non-smokers, chosen at random. No information on their age, gender or 

duration of employment was reported. The control group was 111 males and 

100 females, all non-smokers who worked in areas free of dusts. They were 

20 
said to live in the same area and to be of the same socio-economic status as 

the exposed workers. The method of recruiting the controls was not stated. 

Information on respiratory symptoms was gathered using a modification of the 

MRC and ATS questionnaires and used to identify respiratory conditions 

referred to as chronic cough, chronic bronchitis and bronchial asthma. 

Spirometry was conducted using standard methods for 71 controls and 28 

cement workers prior to commencing a work shift. PEFR was determined 

using a Wright peak flow meter. Current respirable airborne dust 

concentrations were determined from personal air samples. A total of 11 

samples, taken over 6 - 8 hour periods, were analysed. 

The mean dust level (± SD, presumably a 4 - 6 h TWA) for rotary kiln workers 

was 3.2 ± 3.5 mg.m-3 and for packing workers 43.1 ± 35.3 mg.m-3. The 

prevalence of respiratory conditions was significantly higher among the 

cement workers; the percentage of workers in the control and exposed 

groups, respectively, was 9% and 30% with chronic cough, 9 and 26% with 

chronic bronchitis and 8% and 32% with bronchial asthma. The spirometry 

results for the controls and cement dust workers were not presented in a way 

that allowed a comparison. However, it was possible to compare the results 

for 12 operators of the rotary kiln with those for 16 cement packers. Mean 

FVC was similar, FEV1 was slightly lower for the packers (91% vs. 98% of 

predicted) and FEV1/FVC was significantly lower for the packers (90% vs. 

98%). PEFR was lower for the packers, but the difference was not statistically 

significant (92% vs. 98% of predicted). Study shows increased prevalence of 

respiratory symptoms in cement workers, compared with the unexposed 

controls, and poorer lung function test results in the cement workers with the 

highest current dust exposure. 

Abuhaise et al. (1997) investigated the respiratory health of 348 Jordanian cement 

factory workers, who were divided into three groups exposure groups, based on 

current dust exposure measurements. A respiratory questionnaire was administered 

and spirometry was conducted. There was a higher prevalence of asthma in the group 

with the highest dust exposure, but the spirometry results were similar for all three 

groups. 

Pulmonary function and respiratory symptoms were investigated in workers at 

a Jordanian Portland cement-producing factory (Abuhaise et al. 1997). All 

workers employed at the factory for more than 3 years were invited to 

participate; 442 (73%) agreed. After exclusions due to family or preemployment history of respiratory disease, being an ex-smoker (only smokers 

and non-smokers were included), participation in other activities involving dust 

exposure, unacceptable spirometry performance, 348 workers were available 

for study. They were predominantly middle-aged men, with a mean age of 41 

years and most had worked at the plant for between 3 and 14 years. There 

was no unexposed control group. Demographic information and occupational 

and medical histories were collected using a modification of the MRC and 

ATS questionnaire on respiratory symptoms. Spirometry was conducted once 

during a workshift using procedures that were in accordance with ATS 

recommendations. Observed readings were reported as percentage of 

predicted. Current respirable dust exposure levels were measured by 

personal sampling. Between 3 and 5 workers in each of 4 plant areas were 

21 
sampled. Three exposure groups were identified; group 1, the lowest 

exposure group, included administrative and transport workers; group 2 

included maintenance staff, clinker workers and foremen; group 3 included 

packers and cement mill workers. 

The measured geometric mean (± SE) respirable dust concentrations 

(presumably 8 h TWAs) were 0.5 (±2.1), 1.6 (±2.6) and 3.9 (±4.0) mg.m-3 in 

exposure groups 1, 2 and 3, respectively. Overall, 58% of workers reported no 

respiratory symptoms during the last 3 years. The most frequent symptoms 

were cough reported by 19% and dyspnoea by 18%. About 16% were 

considered to have asthma and about 15% were considered to have chronic 

bronchitis (defined as phlegm/cough for at least 3 months each year for at 

least 2 years). The prevalence of asthma was higher in group 3 (27%), but for 

other respiratory symptoms and conditions there were no meaningful 

differences between the groups. Age or duration of employment had no 

influence on questionnaire responses. The prevalence of respiratory 

symptoms was higher among smokers. Mean FEV1, FVC, FEF25-75% and 

FEV1/FVC ratio were similar for all three exposure groups. Overall, this study 

did not provided any convincing evidence that the exposure conditions at this 

factory were causing respiratory problems in the workforce. Because there 

were considerable overlaps in the dust exposure concentration ranges for the 

three study groups the power of the study to detect a dose-response 

relationship would be low. The participation rate of 73% raises the possibility 

that the study population was not representative of the workforce. 

Chanrawanshi and Pati (1996): this study does not contribute any useful information 

on the effects of cement dust. 

PEFR was measured in Indian cement-producing factory workers, with the 

primary aim of assessing the effects of shift work on pulmonary function 

(Chanrawanshi and Pati 1996). The results showed poorer lung function in 

shift workers, but no exposure data was provided and no conclusions 

regarding cement can be drawn. 

Yang et al. (1996) administered a respiratory questionnaire and conducted spirometry 

on 412 Taiwanese cement factory workers. They were exposed to mean respirable dust 

levels of about 4 mg.m-3. The prevalence of respiratory symptoms was higher and FVC 

and FEV1 were reduced, in comparison with controls. 

In Taiwan, pulmonary function and respiratory symptoms were investigated in 

workers at four cement factories (Yang et al. 1996). The study considered all 

male workers who had been employed for more than 5 years at one of these 

factories. After a small number of exclusions because of refusal to participate 

or unacceptable spirometry performance, 412 production workers were 

investigated. Their mean age was 44 years and their mean duration of 

employment was 17 years. A group of 179 administrative workers at these 

plants served as controls. Their ages, duration of employment and prevalence 

of smokers was similar to the exposed group. Demographic information and 

employment histories were obtained by interview. Information on respiratory 

symptoms was obtained using a modification of the ATS questionnaire. 

Chronic bronchitis was defined as cough/phlegm on most days for at least 3 

22 
months of the year. Spirometry was conducted according to ATS 

recommendations. It was not stated if the interviewer and spirometry 

technicians were blinded to exposure status. Current respirable dust exposure 

levels were measured from personal air samples, for persons working in all 

the principal job categories. A total of 198 samples, taken over 4 - 8 hour 

periods, were analysed. 

Geometric mean (± SD) respirable dust concentration for control subjects was 

0.41 ± 0.98 mg.m-3 and for the exposed group, 3.58 ± 4.89 (range 1.28-8.12) 

mg.m-3. The prevalence of cough (19 vs. 12%) and phlegm (18 vs. 13%) was 

significantly higher in the exposed group. However, the prevalence of 

wheezing, dyspnoea and chronic bronchitis was similar in the two groups. 

After adjustment for smoking, age and height, FVC (3.80 l for controls vs. 3.54 

l for exposed), FEV1 (2.98 vs. 2.73 l) and FEV1/FVC (78.42 vs. 77.12%) were 

significantly reduced in the exposed group, in comparison with the controls. 

There were similar reductions in FEF50, and FEF75. The study showed an 

increase prevalence of respiratory symptoms and reduced pulmonary function 

in workers exposed to cement dust. A potential weakness of this study is that 

there may have been socio-economic differences between the cement 

exposed workers and administrative controls, which could have contributed to 

the observed differences between the groups. 

Yang et al. (1993) administered a respiratory questionnaire and conducted spirometry 

on 661 Taiwanese cement factory workers. Current dust measurements were available. 

The prevalence of cough was greater in the group with the highest current respirable 

dust exposure of 1.24 mg.m-3. 

The respiratory health of cement workers at the four plants in Taiwan was 

investigated (Yang et al. 1993). It is possible that some of the respiratory and 

exposure data reported in this publication was also used in the Yang et al. 

(1996) report, summarised above. This earlier report provides information on 

respiratory symptoms and spirometry for 661 cement factory workers. The 

workers were classified into three groups according to respirable dust 

exposure concentration. Group 1 were 146 administrative workers, with mean 

dust exposures of 0.22 (range 0.03-1.4) mg.m-3. Group 2 were 140 

maintenance workers, machine operators and drivers, with mean dust 

exposure of 0.55 (0.13-1.94) mg.m-3. Group 3 were 375 workers in jobs with 

the highest exposures, for example packing or preparing raw materials; mean 

dust concentration was 1.24 (0.38-8.12) mg.m-3. The mean age and duration 

of employment of the three groups were similar, although the percentage of 

smokers was higher in groups 2 and 3. Current respirable dust exposure 

levels were determined by personal breathing zone sampling over 4 to 8 hour 

periods. Between 48 and 78 samples were taken for each exposure group. 

The only indication of a difference in respiratory health between the groups 

was the prevalence of cough, which was higher for group 3 (17% compared 

with 11% for groups 1 and 2); this difference was statistically significant after 

adjusting for smoking. The prevalence of other symptoms, chronic bronchitis 

and spirometry results were similar for all groups. Overall, this study showed 

an increased prevalence of one respiratory symptom (cough) in workers with 

current respirable dust exposure of 1.24 mg.m-3. 

23 
3.4.1.3 Study using chest radiography 

Abrons et al. (1998) conducted chest radiography in 2640 US cement factory workers. 

Information on current dust exposure levels was available. A slight increase in the 

prevalence of minor pulmonary radiographic abnormalities, which seems to be 

confined to current smokers, was observed for the cement workers in comparison with 

blue collar controls. Very few of the cement workers had radiographic findings that 

were indicative of significant pulmonary disease. 

In a cross sectional study, chest radiography was conducted in 2640 randomly 

selected workers from 16 US Portland cement producing factories (Abrons et 

al. 1997). This is a report of an additional investigation conducted on the same 

subjects as a study reported in 1988, which showed no convincing evidence 

of a relationship between cement dust exposure and the presence of 

respiratory symptoms or and changes in pulmonary function (Abrons et al 

1988, cited in HSE 1994). These factories, were a random sample of the 153 

US cement factories. All workers were invited to participate, and 87% agreed. 

The mean age of the exposed group was 41 years, and 95% were male. The 

control group comprised of 1458 blue-collar workers drawn from the food, 

textile and electrical equipment manufacturing industries, judged on the basis 

of workplace inspections by a hygienist not to have been exposed to known 

respiratory hazards. Only 55% of the unexposed workers invited to participate 

agreed. There were age and gender differences in comparison to the exposed 

group; for controls, the mean age was 34 years, and 50% were male. 

Standard posterio-anterior chest radiographs were assessed according to the 

1971 ILO-U/C system, by three independent, qualified, readers. Demographic 

information and medical and employment histories (including information on 

asbestos exposure) were obtained by an interviewer-administered 

questionnaire. Current dust exposure levels were determined by personal fullshift sampling. 

The overall geometric mean levels of respirable (211 samples) and total dust 

(1011 samples) were 0.57 mg.m-3 (range 0.01-46.22) and 2.90 mg.m-3 (range 

0.01-78.61) (presumably an 8 h TWA), respectively. Crystalline silica was 

detected in about 15% of personal respirable dust samples, and levels in 

about 10% of these exceeded a limit of 0.05 mg.m3

. Additionally, no asbestos 

fibres were found in any area air samples taken, or in bulk material samples. 

Radiography revealed low prevalence of abnormalities for both exposed and 

control workers. Rates for both rounded and irregular small opacities 

(category 1 profusion or greater) were about 1% among cement workers 

compared with about 0.1% for the control group. Three cement workers had 

rounded small opacities of category 2; all other cases of opacity were 

category 1. The prevalence of pleural abnormalities was about 1.6% in 

exposed workers and 0.2% in controls. These differences were statistically 

significant, and remained so after adjustment for age and smoking. The 

prevalence of abnormalities for the subset with limited previous exposure to 

other agents was similar to that of the whole group of cement workers. A 

comparison of the findings for this subset with controls by smoking status 

indicated that that the significant differences were confined to current 

24 
smokers. An analysis that took account of duration of employment in current 

and previous current job and cement exposure levels based on current 

measurements indicated a positive relationship between exposure and with 

pleural abnormalities, but not with opacities. 

This study indicates an association between employment in the cement 

industry and a slight increase in the prevalence of minor pulmonary 

radiographic abnormalities, which seems to be confined to current smokers. It 

is noted that very few of the cement workers had radiographic findings that 

were indicative of significant pulmonary disease. Because current exposure 

levels covered such a wide range, and historical exposure data were not 

available, no information on dose-response relationships can be gained from 

this study. 

Laraqui et al. (2001) found a higher prevalence of respiratory symptoms together with 

spirometry deficits among Moroccan concrete manufacturing workers, compared with 

controls. 

Laraqui et al. (2001) investigated the prevalence of respiratory problems in 

workers at two ready-made concrete production plants in Morocco. This study 

is considered briefly, as the workers would have been exposed to gravel and 

sand (and hence silica) as well as to cement dust. The study population was 

120 concrete workers, who were compared with 120 civil servants. No 

quantitative airborne dusts measurements were available. A higher 

prevalence of respiratory symptoms, rhinitis, conjunctivitis and dermatitis was 

reported among the concrete workers. Also, the proportion of workers with 

spirometry deficits, as defined by an official French government grading 

system, was higher among the concrete workers. 

3.4.1.4 Studies investigating symptoms only 

Alvear-Galindo et al (1999) administered a respiratory questionnaire to 425 Mexican 

cement factory workers. A semi-quantitative dust exposure assessment was 

conducted. The prevalence of respiratory symptoms was highest among those with the 

highest exposures. 

The association between levels of exposure to cement dust and respiratory 

symptoms was studied in workers at a Mexican Portland cement-producing 

factory (Alvear-Galindo et al. 1999). The study population was 425 workers at 

a factory, representing 95% of the workforce. Their mean age was 39 years. 

All had worked at the factory for their entire working life. Six semi-quantitative 

levels of dust exposure were established from interviews with a small group of 

experienced workers, taking account of time spent at various work positions 

and the visibility in those areas. Each level was given a score of 1 (the lowest) 

to 6. A list of 85 work positions were drawn up and exposure scores were 

assigned to each position. Information on the work history was obtained by 

questionnaire, and a cumulative exposure score was calculated for each 

worker. It was stated that exposure to other respiratory tract irritants, including 

tobacco smoke, was minimal. Information on respiratory symptoms was 

gathered using the ATS questionnaire. Also, information on respiratory illness 

history was available in personnel records. An occupational health physician 

25 
considered the information from these two sources to make an assessment of 

the presence of respiratory disease. Some workers were said to have 

received compensation for occupational diseases. 

Most workers had been exposed to levels of 4, 5 or 6 for most of their working 

life. Very few workers under the age of 25 reported respiratory symptoms. 

However, 8% of workers aged 25-44 years and 16% aged 45 or more were 

diagnosed with bronchitis; 72% and 83%, respectively, had dyspnoea and 

24% and 32% had wheezing. A diagnosis of ‘occupational respiratory disease’ 

(the diagnostic criteria were not described) was made for 32% and 52% of 

workers from the two respective age groups. The prevalence of respiratory 

problems was greatest among those with the highest cumulative exposure 

scores, after adjusting for age. 

This study reported a high prevalence of respiratory problems at the cement 

factory, which was positively associated with the estimated cumulative dust 

exposure. A limitation to the value of this study is that quantitative exposure 

information was not available. 

Abou-Taleb et al. (1993) administered a respiratory questionnaire to 304 cement factory 

workers in the United Arab Emirates. Chronic bronchitis was present in 12% of 

workers, but there was no control group for comparison. 

The respiratory health of a sample of United Arab Emirates cement workers 

was assessed (Abou-Taleb et al. 1995). From four cement productions 

factories, 304 workers were selected at random. These represented about 

50% of the workers from each factory. Their mean age was 38 years, and 

88% were of Indian nationality. Demographic and lifestyle information and 

medical histories were obtained by interviewer-administered questionnaire. 

Respiratory health problems most frequently reported were chronic cough in 

19% of workers and chronic bronchitis (diagnostic criteria were not stated) in 

12%. Other health problems reported in a minority of workers included 

sneezing with runny or stuffy nose, burning eyes, dermatitis, headache and 

fatigue. Is not possible to draw firm conclusions from this study as it is difficult 

to assess the contribution of cement dust to the reported health problems in 

the absence of either an unexposed group or groups with contrasting dust 

exposure levels for comparisons. 

3.4.1.5 Summary of information on the effects of long-term exposure on nonmalignant respiratory disease 

HSE (1994) noted evidence that repeated exposure to Portland cement has 

produced chronic bronchitis and impaired pulmonary function, but firm 

conclusions could not be drawn because of limitations in the available data. 

The effects of long-term exposure remain poorly studied, particularly because 

there are no longitudinal prospective studies. 

Of the 15 recent studies available, most were cross sectional in design, 

conducted in Portland cement production plants outside of Europe. The 

exception was a retrospective cohort study of a relatively small number of 

26 
Norwegian cement plant workers (Fell et al. 2003). This study provided 

evidence that long-term exposure to an average of respirable dust 

concentration of about 1 mg.m-3 is not associated with deficits in lung function 

or with an excess of COPD. Of the remaining studies, all had significant 

design limitations. Notably, due to the cross sectional design the adverse 

effects of cement may be underestimated because this type of study cannot 

take account of workers that may have left the industry due to work-related 

health problems. Another key weakness of theses studies is that a number 

lacked quantitative exposure data and none included historical exposure data. 

Nevertheless, many of these studies provide a consistent picture of the 

presence of respiratory symptoms, reports of bronchitis, and pulmonary 

function deficits in workers exposed to cement plant dust. Typical symptoms 

associated with cement plant work were cough, phlegm and dyspnoea. 

Deficits of lung function were usually seen as a reduction in FEV1, FVC and 

FEV1/FVC ratio, suggesting an obstructive impairment. In studies that 

provided some information on dust exposure conditions, the lowest current 

dust exposure concentrations associated with poorer lung function were about 

3 mg.m-3 total dust (Mwaiselage et al 2004), or about 2 - 4 mg.m-3 respirable 

dust (Noor et al. 2000, Yang et al 1996). The lowest concentration associated 

with in increase in respiratory symptoms was 1.2 mg.m-3. However, no reliable 

conclusions about dose-response relationships can be drawn because of the 

limitations of these studies. Nevertheless, the evidence provided by the recent 

studies qualitatively strengthens the picture presented in the earlier HSE 

(1994) review. 

Overall, the pattern of evidence clearly indicates that occupational exposure to 

cement dust has produced deficits in respiratory function. However, the 

evidence available at the present time is insufficient to establish with any 

confidence the dose-response relationship for these effects. 

27 
3.4.2 Mortality and cancer studies involving workers with long-term 

exposure to cement dust 

HSE (1994) concluded that mortality studies conducted on cement workers 

provided no evidence of increased incidence of death from non-malignant 

respiratory disease. With regard to cancer, three cohort mortality studies 

conducted in cement manufacturing workers found elevated SMRs for 

stomach cancer. The elevation was statistically significant in one study 

conducted in the UK (SMR 1.75, based on 22 observed deaths,). In other two 

studies the SMRs were not statistically significant (SMR 1.19 based on 24 

deaths and SMR 1.35 based on 27 deaths). Several other studies found 

associations between exposure to cement and various site-specific cancers 

but these were isolated reports and no firm conclusions could be drawn. 

Overall, HSE (1994) came to the view that there was no convincing evidence 

for an increased incidence of any site-specific cancer resulting from exposure 

to cement dust, but it was also acknowledged that the results emerging from 

the studies available up to 1991 were not consistently and reassuringly 

negative. 

Since 1991, a number of mortality and cancer cohort studies conducted in 

cement production workers of cement masons have been conducted. Also, a 

series of case control studies conducted in Germany have drawn attention to 

occupational contact with cement as a possible risk factor for cancers of the 

oral cavity, pharynx and larynx. The present review also briefly considers 

earlier case control studies that have investigated risk factors for laryngeal 

cancers, and other recent cancer related studies that include subjects that 

may have been exposed to cement. 

3.4.2.1 Mortality and cancer cohort studies in cement production workers or 

masons 

Recent cohort studies conducted in cement production workers in three 

northern European locations, in Sweden, Denmark and Lithuania, are 

available. Additionally, a cancer cohort study has been conducted in Icelandic 

cement masons. These studies are appraised below, and summarised in 

Table 2. 

Jakobsson et al. (1993) investigated mortality and cancer morbidity in about 2400 

Swedish cement factory workers. Overall mortality and cause-specific non-malignant 

mortality for the cement workers were similar to the national rates. However, the 

analysis of individual tumour sites revealed an increased risk of tumours of the right 

side of the colon (SIR 2.7, 95% CI 1.4 - 4.8, 12 cases). The risk was increased among 

those with more than 25 years cement plant work. 

In a retrospective cohort study mortality and cancer morbidity experiences of a 

group of about 2400 workers at two Swedish cement production factories 

were investigated (Jakobsson et al. 1993). This study was conducted as a 

follow up to the Jakobsson et al. (1990) case control study summarised by 

HSE (1994), which reported an increased risk of colorectal cancer associated 

with one of the cement factories (factory A). The cohort consisted of all men 

employed at the factories at the start of January 1952 or since then, and with 

28 
a total employment of at least one year. Mortality and cancer morbidity 

information to the end of 1986 was obtained from death certificates and a 

national tumour registry and compared with the age-adjusted rates for the 

general population of Sweden (mortality) or the regions in which the plants 

were located (morbidity). About 90% of the cancers diagnoses were confirmed 

by histology or cytology. The analysis focused on cancers occurring 15 years 

or more after commencement of exposure. 

Very limited exposure data were available. The report states that new cement 

ovens and automatic process controls were introduced at both plants during 

the 1960s and ventilation was improved during the 1970s suggesting that dust 

exposure during the latter years of the study period were considerable lower 

than earlier. At factory A, total dust measurements made from the mid-1970s 

onwards were generally lower than 10 mg.m-3 (presumably as a TWA). Dust 

surveys conducted in factory B during the early 1970s showed that total dust 

airborne concentrations were generally less that 20 mg.m-3 and in later years 

less that 10 mg.m-3. Concentrations greater than 100 mg.m-3 were found for 

some cleaning and maintenance tasks, although it was suggested that 

respiratory protection might have been used during these operations. Factory 

B measurements were based on personal sampling and expressed as a TWA, 

although the sampling time was not stated. The quartz content of the dust was 

said to be generally less than 5%, and no cases of silicosis have been 

reported at these plants. 

Overall mortality (495 observed deaths vs. 527 expected) and cause-specific 

non-malignant mortality for the cement workers were similar to the national 

rates. Also, overall tumour morbidity (162 observed cases vs. 160 expected) 

did not differ from the regional rates. However, the analysis of individual 

tumour sites revealed a significant increased risk of tumours of the right side 

of the colon (SIR 2.7, 95% CI 1.4 - 4.83, 12 cases). The risk was increased 

among those with more than 25 years cement plant work (SIR 4.3, 95% CI 1.7 

- 8.9, 7 cases). However, the risk of right-sided colon cancer was not 

significantly increased at factory A, which was associated with an excess of 

colorectal cancer morbidity in the Jakobsson et al report of 1990. All colon 

cancer cases had been confirmed by histology or cytology. There was no 

excess of tumours at other sites. The authors discussed the possibility of bias 

due to the use of an inappropriate reference population. Farmers are known to 

have very low rates of colon cancer and a relatively high proportion of farmers 

in the localities of the cement plants may have resulted in a bias of the 

magnitude of the calculated SIR in the direction of an overestimate. 

As an extension to their 1993 study, Jakobsson et al. (1994) reanalysed mortality and 

cancer morbidity for the 1520 Swedish cement factory workers. Comparisons with 

other groups of blue-collar workers and with the general population were conducted. 

An increased risk of cancer of the right side of the colon (SIR 2.6, 95% CI 1.4 - 4.6) for 

the cement workers was confirmed. 

In a later report, the risk of right-sided colon cancer at the two Swedish 

cement factories was compared with that for asbestos cement workers, other 

industrial workers without significant exposure to mineral dust or fibres and 

fishermen in Sweden (Jakobsson et al. 1994). All members of the 

29 
occupational groups had a minimum employment of one year, and only 

cancer morbidity occurring more than 15 years after the commencement of 

employment was considered. Cancer mortality and morbidity for the period 

1958 to about 1987 (slightly later for fishermen) was ascertained and SMRs 

and SIRs were calculated with reference to the general male population of 

Sweden. The cohort of cement workers consisted of 1526 blue-collar workers 

with a median birth year of 1927. The asbestos cement cohort was 981 bluecollar workers from a building materials factory, with median birth year 1913. 

The ‘other’ industrial workers cohort consisted of 3965 blue-collar workers 

from a variety of industries where some chemical exposures were likely. The 

cohort of fishermen was 8092 in number, with a median birth year of 1924. 

Overall cancer mortality for the cement workers was similar to the general 

population (SMR 1.02, 95% CI 0.92-1.25), and to ‘other’ industrial workers. 

The cancer mortality for the asbestos workers was slightly higher, and for the 

fishermen slightly lower. Morbidity from right-sided colon cancer was 

increased among cement workers (SIR 2.61, 95% CI 1.35-4.57), but risk of 

left-sided colon cancer was not increased. The findings for asbestos cement 

workers were similar. Morbidity for colon cancers among the ‘other’ industrial 

workers and fishermen was similar to the general population. This study 

showed an increased risk of right-sided colon cancer among workers with 

long-term exposure to cement dust compared to other blue-collar workers, 

which constitute an appropriate reference population, and to the general 

population. 

Vesbo et al. (1991) investigated cancer morbidity in 546 Danish cement factory 

workers. No evidence of an increased risk of cancer was reported, when compared 

with a control group drawn from the local population. 

The relationship between employment at a Danish Portland cement factory 

and cancer morbidity was investigated in a cohort study (Vesbo et al. 1991). 

The cohort of cement workers comprised of all men aged 46-69 living in the 

city of Aalborg who had worked at the factory for at least one year prior to 

1974; there were 546 men meeting these criteria. The control group was all 

men of the same age group living in this city who had not worked at the 

factory for a year or more and who were born on the 1st or 15th of each 

month; they numbered 856. Information on employment and lifestyle factors 

was gathered by questionnaire. From factory personnel records, the cement 

workers were classified as having either 1-20 years or ≥ 20 years 

employment. Information on actual occupation within the factory was not 

available so it was not possible to categorise individuals into more precisely 

defined exposure groups. The control subjects were categorised into three 

occupational groups, blue-collar workers, white-collar workers and ‘others’. 

Information on cancer cases for the period 1974 to 1985 was obtained from 

the Danish Cancer Registry. The numbers of observed cases of cancer for 

each study group were compared to the expected number based on cancer 

incidence rates for the relevant age groups for the total male population of 

Denmark. 

Airborne cement dust measurements were not made prior to 1974. Personal 

sampling during 1974 showed that 9% of respirable dust measurements were 

30 
greater than 5 mg.m-3. No increased risk of all types of cancer was seen 

among cement workers compared with either the general male population or 

with each of the control groups. However, the risk of respiratory cancer was 

higher among cement workers when compared to the general male 

population. The authors provided a more detailed comparison of the risk of 

respiratory cancer for cement workers and white-collar controls, after 

excluding all men with asbestos exposure due to employment at a nearby 

asbestos-cement plant (approximately 5% of cement workers) and controlling 

for age and smoking. The RRs for respiratory cancer were 0.5 (95% CI 0.1-

1.5) for men with 1-20 years cement factory employment and 1.0 (95% CI 0.4-

2.6) for men with ≥20 years employment. The authors pointed out a drawback 

with respect to comparisons with the blue-collar control group, since members 

of this group may have been exposed to asbestos at a large local shipyard. 

Overall, this study provides no convincing evidence of an increased risk of 

cancer morbidity associated with cement dust exposure at the cement factory. 

Smailyte et al. (2004) investigated mortality and cancer morbidity in 2500 Lithuanian 

cement factory workers. There was an increased incidence of lung cancer among 

cement workers (SIR 1.5, 95% CI 1.1-2.1) compared to the general population, but 

smoking was not taken account of in the analysis. A dose-related trend towards an 

increased incidence of stomach cancer was observed, although the number of cases 

was small. 

In a cohort study, mortality and cancer incidence among workers at a 

Lithuanian Portland cement producing plant was investigated (Smailyte et al 

2004). The study population comprised all workers employed by the cement 

producing departments for at least 12 months between 1956 and 2000 and 

who were available for the follow-up period of 1978 to 2000. The study 

population numbered 2498, which was about 94% of all those who had 

worked at the plant from 1978 to 2000. This cohort represented 43490 person 

years of exposure. Approximately 70% of the study population were men. 

Subjects were identified from factory records, which provided information on 

age, employment start and finish dates, and factory departments in which 

each subject worked. Information on vital status, cause of death and cancer 

cases were obtained from Government population registers, death certificates 

and the Lithuanian Cancer Registry. SIRs and SMRs were calculated with 

reference to the gender and age-adjusted rates for the general Lithuanian 

population. 

Some dust exposure information was available from 1975, expressed as 

annual mean total dust concentrations. These were calculated from static 

sampling measurements (sampling time was not stated) conducted four times 

a year in various departments. Annual mean dust concentrations were highest 

in the packing (ranging from 19.1 to 15.0 mg.m-3) and calcining (19.2 to 8.2 

mg.m-3) departments. 

The overall mortality among male cement workers was not increased (376 

observed deaths, SMR 1.0, 95% CI 0.9-1.1), but deaths from malignant 

neoplasms were increased (102 observed, SMR 1.3, 95% CI 1.0-1.5), mainly 

due to lung cancer mortality (SMR 1.4, 95% CI 1.0-1.9). There was no excess 

mortality for non-malignant respiratory disease. Among females, overall 

31 
mortality and mortality for specific causes was similar to that of the general 

Lithuanian population. The cancer incidence data for male cement workers 

revealed a slight excess for all malignancies (SIR 1.2, 95% CI 1.0-1.4). The 

only site showing a significant excess was the lung (SIR 1.5, 95% CI 1.1-2.1). 

A total of 389 cement workers had been also been involved with the 

production of asbestos cement at another plant in the same area. When these 

were excluded from the analysis the incidence of lung cancer remained 

elevated (SIR 1.4, 95% CI 1.0-2.0). There was a slight trend towards an 

increased incidence of lung cancer with increasing time since first 

employment and duration of employment. The authors presented cancer SIRs 

for categories of cumulative dust exposure, but it was not clear from the report 

how this index of exposure was calculated. There was no obvious relationship 

between lung cancer and cumulative exposure, although the SIRs were 

significantly increased for the two highest dust exposure categories 

designated ‘55-130 mg.m-3 year’ (SIR 2.0, 95% CI 1.2-3.4) and ‘>130 mg.m-3 

year’ (SIR 1.8, 95% CI 1.1-3.0). The authors of the study drew attention to an 

increase in the incidence of cancers of the urinary bladder, but the increase 

was not statistically significant (8 cases, SIR 1.8, 95% CI 0.9-3.5) and there 

was no convincing relationship with duration of employment of cumulative 

dust exposure. There was a trend towards an increased incidence of stomach 

cancers with cumulative dust exposure; for a ‘55-130 mg.m-3 year’ exposure 

group the SIR was 1.1 (4 cases, 95% CI 0.4-2.8) and for a ‘>130 mg.m-3 year’ 

exposure group the SIR was 1.5 (6 cases, 95% CI 0.6-3.0). 

The authors discussed a major limitation of this study, which is that no data on 

tobacco consumption was available. It was stated that about half of the male 

population of Lithuania are smokers, and it is likely that more blue-collar 

workers smoke than white-collar workers. Therefore it is possible that the 

results of this study may have been subjected to a confounding influence of 

smoking. If the analysis had taken account of smoking, the statistically 

significant differences observed for the SIRs for lung cancers in this study 

may have been eliminated. For this reason it is not possible to draw 

conclusions about the role of cement dust in reported increase in the risk of 

cancers. It is noted that due to the crude nature of exposure assessment there 

is a high potential for exposure group misclassification, which could result in 

the masking of any dose response relationships. 

Rafnsson et al. (1997) investigated cancer in 1172 Icelandic cement masons. The study 

revealed an increased risk of lung cancer among the masons in comparison with the 

general population of Iceland (SIR 1.7, 95% CI 1.1-2.5). The SIR was increased when the 

analysis allowed for a latency period of 30 years from the start of work as a mason. 

Rafnsson et al. (1997) conducted a retrospective cohort cancer study in all 

1172 Icelandic licensed masons who were born after 1880 and alive in 1955. 

The cancer experiences from 1955 to 1993, or until death if before 1993, were 

ascertained from the national Cancer Registry. It was possible to obtain 

information on the status of all study subjects. Most of the cancer cases had 

been verified by histological diagnosis. Masons alive at the time of the study 

were questioned on their smoking habits and the number of years worked as 

a mason. The main task of the masons was to finish and smooth the surfaces 

of concrete structures using wet concrete, applied by trowel or by spraying. 

32 
No quantitative exposure data were available, although it was stated that 

when spaying inside a thick mist of an aerosol of concrete was produced that 

made it difficult to see across the room. Dermal contact with the wet concrete 

was described as ‘intensive’ on hands and face. The concrete contained 

cement, sand, water and other compounds. A survey showed that about 88% 

of responding masons had worked as finishers for at least 10 years. 

The study showed an increased risk of lung cancer in comparison with the 

general population of Iceland (SIR 1.69, 95% CI 1.09-2.49). The SIR was 

increased when the analysis allowed for a latency period of 30 years since 

completing vocational training (SIR 1.77, 95% CI 1.01-2.88). The percentage 

of never-smokers among the masons was estimated to be lower than in the 

general population, but this could not account for the increased risk. For all 

other tumour sites there were no increased risks for the cement masons. The 

masons would have been exposed to silica, but there were no identified cases 

of silicosis. Strengths of the study are that the design provided protection 

against subject selection bias, cancer ascertainment was reliable and 

complete, and the follow-up period was long. However, weaknesses of the 

study are that exposure information was not available and an analysis of 

cancers in relation to duration of employment was not conducted. 

33 
3.4.2.2 German case control studies for cancers of the oral cavity, pharynx 

and larynx 

Maier et al. conducted a series of population-based case control studies in 

cancer patients from the Gliessen and Heidelberg University Ear Nose and 

Throat (ENT) clinics investigating occupational and other risk factors for 

cancers of these sites. These studies are appraised below, and summarised 

in Table 3. 

Maier et al. (1991) investigated the occupational risk factors for cancers of the oral 

cavity, pharynx and larynx in 200 cases and 800 controls. The study reported an 

elevated risk of cancer associated with occupational exposure to cement. The 

estimated RR was 2.4 (95% CI not stated) after adjustment for smoking and alcohol 

consumption. 

In the first study the occupational exposure histories of cases of squamous 

cell carcinomas of the oral cavity, oropharynx, hypopharynx and larynx were 

investigated (Maier et al. 1991). The investigations were conducted at the 

Gliessen University ENT Clinic and the Heidelberg University ENT clinic. The 

same patients were investigated in an earlier study, in which non-occupational 

risk factors for cancers at these sites were analysed (Maier et al 1990). The 

first 100 patients with the above diagnosis attending each clinic for 

consultation or treatment from September to December 1987 (Gliessen) or 

February 1988 to April 1988 (Heidelberg) were selected for each study. 

Patients who were first diagnosed more than three years prior to the study 

period were excluded. The Gliessen control group consisted of 400 male 

patients attending either the ENT (200 patients) or Medical (200 patients) 

Clinics of Gliessen University who had no known cancer. Four controls were 

assigned to each case, two from each of the ENT and Medical Clinics, who 

were matched for age (± 2 years) and size of their home. The selection or 

number of Heidelberg controls was not described in detail, although the 

design of this part of the study was said to be similar to that of the Gliessen 

study. Approximately 30% of Gliessen case and control patients and 20% of 

Heidelberg case and control patients who were invited to participate in the 

study declined. 

Occupational exposure information for each of the Gliessen patients was 

obtained by one interviewer using a computerised questionnaire that focussed 

mainly on exposures to harmful substances at work. Patients were asked 

simply whether or not they had been exposed to asbestos, welding gases, 

organic compounds, heavy metals, coal products, wood dust, cement, 

herbicides and ionising radiation. No information on duration or frequency of 

exposure was collected. Details of the method of collecting exposure 

information for the Heidelberg patients was not described in detail, except it 

was mentioned that information of duration of exposure was collected and the 

analysis included only substances to which the patient had been in contact 

with for at least once a week for more than 10 years. It was not stated if the 

interviewer was blinded to case/control status, or if the patients were aware of 

the purpose of the investigation. The analysis of the results of the Heidelberg 

study included an adjustment for the influence of alcohol consumption and 

smoking. RRs for occupational risk factors were estimated from odds ratios. 

34 
The majority of cases were within the age range 49 to 66. The distribution of 

tumour sites was similar for both study centres; approximately 45% were 

carcinomas of the larynx, 23% of the oral cavity, 24% of the oro-pharynx and 

8% of the hypo-pharynx. 

The exposure information for the Gliessen and Heidelberg study centres was 

analysed separately. For the Gliessen study, the percentage of cases with 

cement exposure was significantly higher than controls (14.5% of controls vs. 

25% of cases). The percentage of cases with asbestos exposure was also 

significantly higher than controls (22% vs. 40%). There were no differences 

between the cases and controls for the other exposures. For the Heidelberg 

study, the proportion of cases with occupational exposure to cement 

(estimated RR 4.4, 95% CI 2.4-8.4), organic compounds, wood dust or coal 

products were significantly greater than controls. After adjustment for the 

effects of alcohol and tobacco only the estimated risks for cement remained 

statistically significant (RR 2.4, 95% CI not stated). The RRs for cement 

increased with duration of exposure; compared with that for less than 5 years 

exposure, the estimated RR was almost 3 times higher for 5-20 years 

exposure, 5.5 times higher for 20-40 years, and 6.3 times higher for more than 

40 years. However, the confidence intervals of the estimated RRs for these 

subgroups were not reported, neither were the number of cases within each 

exposure band, so it so it is not possible to assess the robustness of this 

trend. 

A limitation of the Gliessen study is that the exposure assessment identified 

anyone who had come into contact with a particular substance at any time 

during their work; the authors consider this part to be a pilot exercise for the 

Heidelberg study. The Heidelberg study provides evidence of an association 

between cement exposure and cancer of the upper respiratory/digestive tract. 

As with many case control studies, the exposure assessment relied on the 

recall of the subjects, which may be subject to bias because the cases may 

have a greater motivation to recall chemical exposures than the control 

patients. Such a bias would result in an overestimation of risks associated 

with cement exposure. Similarly there may have been interviewer bias in that 

the interviewer may have pressed harder to gain information on occupation 

exposure for the cases. However, there is no logical reason for the cases to 

be more strongly motivated to recall cement exposure in preference to 

exposures to other substances, unless they were aware of a hypothesis that 

cement exposure was associated with cancers of the upper 

respiratory/digestive tract. 

Maier et al. (1992) investigated the occupational risk factors for cancers of the larynx in 

164 cases and 656 controls. The study reported a slightly elevated risk of cancer 

associated with occupational exposure to cement. The estimated RR was 1.2 (95% CI 

0.9-1.4) after adjustment for smoking and alcohol consumption. 

Maier et al. (1992) investigated the occupational exposure risk factors 

associated with squamous cell carcinoma of the larynx. The cases, numbering 

164, were all male patients attending the Heidelberg University ENT clinic with 

this diagnosis during the periods June 1988 to October 1988 and November 

35 
1988 to April 1989, excluding those first diagnosed more than 3 years prior to 

the study periods. The controls were 656 male patients without a cancer 

diagnosis, half of whom attended the Heidelberg University ENT and half from 

the Medical Out-Patients Department of the University Clinic. Four controls 

were assigned to each case, two from each of the ENT and Medical Clinics, 

who were matched for age (± 2 years) and size of their home. No information 

on the numbers of available cases and controls refusing to participate was 

given. Occupational and personal information was collected by interview using 

a computerised questionnaire. The subjects were said to have been 

questioned on extent and duration of exposure to potentially harmful 

materials, but no detailed information on the questions, or interview conditions 

were given. RRs for occupational risk factors were estimated from odds ratios. 

Regarding the types of laryngeal cancers among the cases, 72 were glottal 

cancers, 73 were supraglottal, and 19 could not be classified. Several 

indicators of the level of education showed that average level of education 

was noticeably higher for controls; for example 90% of cases had no schoolleaving certificate, compared with 74% of controls. After adjusting for alcohol 

and tobacco consumption, a significantly elevated estimated RR was found 

only for cases reporting occupational exposure to coal/coal tar products 

(estimated RR 2.67, 95% CI 1.3-5.5). The risk associated with cement 

exposure showed a marginally statistically significant elevation (estimated RR 

1.4, 95% CI 1.1-1.6) but the risk was not statistically significant after 

adjustment for alcohol and tobacco consumption (estimated RR 1.18, 95% CI 

0.9-1.4). 

This study points to the possibility of an association between exposure to 

cement and cancer of the larynx. As for the Maier et al 1991 study, the 

exposure assessment relied on the recall of the patients, which may have 

been subject to bias. 

An analysis of data from what is presumed to be the same group of cases and 

controls investigated in the above study was included in a later publication 

(Maier and Tisch 1997), but this report did not provide any additional 

information on the risks of laryngeal cancer associated with cement exposure. 

Maier et al. (1994) investigated the occupational risk factors for cancers of the pharynx 

in 105 cases and 656 controls. An elevated risk of cancer associated with occupational 

exposure to cement was reported. The estimated RR was 2.2 (95% CI 0.9-5.2) after 

adjustment for smoking and alcohol consumption. 

In another case control study, the occupational exposure risk factors for 

pharyngeal cancer were investigated (Maier et al. 1994). The cases were 105 

male patients with histologically confirmed cancer of the pharynx who 

consecutively attended the University of Heidelberg Department of Otorhinolaryngology/Head and Neck Surgery during the period February 1991 and 

mid-September 1991. The controls were 656 male patients without a cancer 

diagnosis, half of whom attended the Heidelberg University ENT and half from 

the Neurological Clinics. Four controls were assigned to each case, two from 

each of the ENT and Neurological Clinics, who were matched for age (± 5 

years) and size and location of their home. Personal and occupational 

36 
information was obtained by interview, all of which were conducted by the 

same interviewer. In comparison with the earlier Maier studies, more detailed 

employment information, including the time spent working on particular 

activities, was gathered. Each subject was asked if they had been exposed, 

and for how long, to a number of specific materials/activities, including 

asbestos, welding fume, particular metals, cement, coal tar products, types of 

wood dust, herbicides, biocides, lubricants and general dusts. RRs for 

occupational risk factors were estimated from odds ratios. 

The percentage of cases that were construction workers was 27%, compared 

to 7% of controls (estimated RR 4.9, 95% CI 1.3-5.9). Alcohol and tobacco 

consumption was much higher among cases that were construction workers 

than controls who were construction workers. There was a similar difference 

in alcohol and tobacco consumption among cases and controls from other 

occupations. After adjustment for alcohol and tobacco consumption, the RR 

estimate for construction workers for the risk of pharyngeal cancer was 2.8 

(95% CI 1.1-5.9). When the analysis focused on long-term (more than 10 

years) occupational contact with cement the estimated RR was elevated, at 

2.2 (95% CI 0.9-5.2) after adjustment for alcohol and tobacco. The 29 cementexposed cases had a mean duration of contact with this material for 25 (SD 

9.3) years. Thus, this study demonstrates an increased risk of pharyngeal 

cancer among construction workers with long-term contact with cement, but 

when tobacco and alcohol consumption are taken into account this increased 

risk was not statistically significant. Overall, this study points to the possibility 

of an association between exposure to cement and pharyngeal cancer. As for 

the previous Maier studies, the exposure assessment relied on the recall of 

the patients, which may have been subject to bias. 

Maier et al. (1999) presented an overview of the results of their cancer case 

control study series (Maier et al. 1991, 1992 and 1994). There was no 

additional information on cancer risks for cement-exposed workers in this 

report. 

Maier et al. (2002) investigated the occupational risk factors for cancers of the oral 

cavity, pharynx and larynx in 206 cases and 110 controls, matched for smoking and 

alcohol consumption. A substantially increased risk of cancer associated with 

occupational exposure to cement was reported. The OR was 12.6 (95% CI 3.9-43.0) after 

adjustment for smoking and alcohol consumption. 

In the most recent Maier study, occupational and nutritional risk factors for 

cancers of the oral cavity, pharynx and larynx were investigated in cases 

matched to controls with similar alcohol and tobacco consumption (Maier et al. 

2002). The cases were 209 male German patients with histologically 

confirmed squamous cell carcinoma at these sites attending the Heidelberg 

University ENT clinic. The control subjects were 110 male German patients 

attending the ENT clinic without a cancer diagnosis and matched to the cases 

for age, alcohol consumption and tobacco consumption. Recruitment took 

place over a 5-year period, between 1990 and 1995. No further details of the 

case and control subject selection procedures were described, so it is not 

possible to assess if these procedures introduced bias. The report stated that 

access to non-cancer patients with high alcohol and tobacco consumption 

37 
was restricted and a willingness of these patients to cooperate was low. It was 

not stated whether or not any of the cases or controls were included in the 

studies reported earlier. Occupation and medical histories, and information on 

alcohol/tobacco consumption, nutrition and socio-economic factors were 

gathered by interview with the aid of a standardised questionnaire. Specific 

questions were asked about exposures to asbestos, organic solvents, heavy 

metals, coal products, wood dust, cement, herbicides and ionising radiation. In 

the analysis only those occupational substances to which a subject was in 

contact with at least once a week for more than 10 years was taken into 

account. It was not stated if the interviewer was aware of the subject 

case/control status. 

The age distribution of cases (56 ± 9 years) and controls (58 ± 10) was 

similar. The level of educational attainment of the controls was higher, for 

example 10% of the cases and 29% of the controls attended further education 

institutes (such as trade school, technical college or university). The 

prevalence and type of non-cancer diseases present among the cases and 

controls were similar. Mean alcohol consumption for the cases (86 ± 64 g/d) 

and controls (97 ± 60 g/d) was similar, as was tobacco consumption (49 ± 30 

pack years for cases, 56 ± 37 pack years for controls). The percentage of 

cases with an occupation in the construction or demolition industries was 

21%, noticeably higher that the 7% of controls. When contact with individual 

occupational materials were considered, regular contact with two materials 

showed significantly elevated odds after adjustment for alcohol and tobacco 

consumption: asbestos (OR 8.7, 95%CI 2.0-37.0) and cement dust (OR 12.6, 

95% CI 3.9-43.0). 

The high OR for cement dust exposure indicated a strong association with 

cancers of the head and neck. A potential weakness of this study is that that 

the cases and controls did not appear to be comparable in terms of education, 

suggesting there were socio-economic differences between the two groups. 

This potential confounding factor was not taken account of in the analysis. 

Also, there may have been bias in the selection of controls resulting from a 

lack of willingness of potential controls to participate. The extent and direction 

of this bias cannot be assessed from the information presented in the report. 

However, the magnitude of the OR is such that confounding and bias cannot 

be the only explanation for its elevation. 

Dietz et al. (2004) investigated the occupational risk factors for cancers of the larynx in 

257 cases and 769 population controls. An elevated risk of cancer associated with 

occupational exposure to cement was reported. The OR was 1.18 (95% CI 0.77-1.18) 

assessed by substance questionnaire or 2.04 (95% CI 1.16-3.56) assessed by jobspecific questionnaire, after adjustment for smoking, alcohol consumption and socioeconomic status. 

In a very recent case control study (known as the ‘Rhein-Neckar-Larynx 

Study’) the occupational risk factors associated with squamous cell carcinoma 

of the larynx were investigated (Dietz et al. 2004). Eligible cases were all 

patients attending the Otolaryngology, Head and Neck Surgery departments 

of the Heidelberg, Mannheim, Ludwigshafen, Darmstadt and Heilbronn 

hospitals with a new, histologically confirmed, diagnosis of cancer of the 

38 
larynx between May 1998 and December 2000. All laryngeal cancer patients 

from the study region are treated at these hospitals. Of the eligible cases, 257 

(96%) agreed to participate. Three control subjects, matched for age, gender 

and residential location, were assigned to each case. Controls meeting the 

matching criteria were chosen at random from population registries. Of the 

1233 control subjects selected, 769 (62%) agreed to participate. The age 

range of participants was 40-75 years. 

Information on occupational exposures and other risk factors was obtained by 

face-to-face interview, using standardised questionnaire. Five interviewers, 

with special questionnaire training, were used. All cases, and 554 of the 

controls were interviewed at one of the participating hospitals. An 

occupational history of jobs held for more than 6 months was obtained, and 

subjects were asked if they had been exposed to a checklist of named 

substances that the authors considered to be either known or suspected 

respiratory carcinogens. Detailed information on exposures was obtained by 

supplementary job-specific questions, which was used to assign semiquantitative exposure scores. Detailed information on smoking and alcohol 

consumption was also gathered. As a validation exercise, a special cement 

questionnaire was administered about 2-4 years after the original interview to 

subjects thought to have experienced cement exposure. Information on the 

techniques used, the types of cement used, the methods of processing 

cement products on-site, and for exposures to asbestos and asbestos cement 

was requested. Because of death, loss of contact or refusal, only 26% of 

eligible cases and 75% of eligible controls participated in the validation 

exercise. 

Smoking was found to be a very significant risk factor for laryngeal cancer. 

The OR for heavy smokers was 32.5 (95% CI 15.1-71.0), after adjustment for 

alcohol consumption. High alcohol consumption was also a risk factor, shown 

by an OR 2.4 (95% CI 1.5-9.7) for those consuming more than 75g alcohol 

per day, after adjustment for tobacco consumption. The occupation risk factor 

analysis focussed on cement exposure. One analysis was based on the 

carcinogenic substance questionnaire responses; 23.3% of cases claimed 

cement exposure compared to 14.4% of controls (OR 1.18, 95% CI 0.77-1.18, 

after adjustment for alcohol, tobacco and socio-economic status). A second 

analysis considered the responses to job-specific questions and found fewer 

cases and controls judged to have experienced cement exposure; 14.8% of 

cases had been exposed, compared to 5.1% of controls (OR 2.04, 95% CI 

1.16-3.56, after adjustment). However, there were no indications of a doseresponse when the ORs were calculated for low (less than 3000 cement 

working hours) and high (more than 3000 hours) exposure groups; the OR 

(after adjustment) for the low exposure group was 2.22 (95% CI 1.02-4.48) 

and for the high exposure group 1.87 (95% CI 0.88-4.01). 

In the validation exercise, cement exposure of the 15 participating cases was 

confirmed, but cement exposure was confirmed for only 69/80 (86.3%) of 

controls, suggesting that cement exposure for the controls may have been 

overestimated. This analysis also showed that more cases had also been 

exposed to slaked lime (which was sometimes used in place of Portland 

39 
cement in the 1950s and early 1960s), but the numbers of subjects was too 

few to draw any conclusions. 

Overall, the results of this study provide evidence of an association between 

exposure to cement and laryngeal cancer. However, this association appears 

weak as a dose response could not be detected and ORs, at the most, were 

only marginally statistically significant. As for the Maier studies, the exposure 

assessment relied the recall of the subjects, which may have been subject to 

bias in favour of recall of cement exposure by the cases. 

3.4.2.3 Earlier case control studies investigating risk factors for laryngeal 

cancers 

Earlier studies of risk factors for laryngeal cancers, identified from a PubMed 

search of literature published from 1980, have been briefly considered to 

determine whether there is corroborative evidence for the association 

between cement exposure and cancers at this site observed in the German 

studies. Six such studies were found, which are summarised below. 

In a Danish study, 326 cases of newly diagnosed laryngeal cancer were 

investigated (Olsen and Sabroe, 1984). For each case four control subjects, 

matched for age and gender were identified from local person-registration 

lists. Information on occupational history, occupational exposures, alcohol and 

tobacco consumption was obtained by postal questionnaire. All RRs, 

estimated from odds ratios, were adjusted for age, alcohol and tobacco 

consumption. The RR for laryngeal cancer in unskilled/semiskilled workers 

was significantly elevated (RR 1.8, 95% CI 1.3-2.6). The RRs for skilled and 

salaried workers or professionals were not elevated. Of the occupational 

materials, the RR was elevated only for ‘any occupational dust’ (RR 1.6’ 95% 

CI 1.2-2.0). The RR for exposure to cement was not elevated, at 0.9 (95% CI 

0.6-1.3, 42 cases, 148 controls). Among 7 occupations listed with significantly 

elevated RRs was employment in concrete, cement and asbestos cement 

manufacture (RR 17.3). This RR related to just 6 cases and 2 controls. As 

this grouping included asbestos cement workers, and involved a small number 

of subjects, no conclusions about cement dust can be drawn from this 

observation. 

Cauvin et al. (1990) studied all 2471 cases of squamous cell cancer of the 

oropharynx, hypopharynx, glottis, supraglottis, epilarynx and oral cavity 

identified at a Paris hospital between 1975 and 1984. The controls were 147 

males, who were all patients attending the hospital during the study period 

who were healthy or with a cancer at another site. Information on occupational 

history, occupational exposures and alcohol and tobacco consumption was 

obtained by interview. The OR for the exposure category of ‘cement, stone’ 

was significantly elevated for cancers at only one of nine sites analysed, the 

supraglossis. After adjustment for alcohol and tobacco consumption the OR 

was 2.4 (95% CI 1-5.8). However, this could be a chance finding as elevated 

risk was limited to one tumour site. The exposure group included exposure to 

stone, so the role of cement dust exposure is even more uncertain. 

40 
The possible occupational risk factors for laryngeal cancer were investigated 

on the Texas Gulf Coast (Brown et al. 1982). The cancer cases were obtained 

from hospital records and tumour registries at 56 (out of possible 67) hospitals 

in the study area. All diagnoses of laryngeal cancer for white males aged 30 to 

79 living in the study area during the period mid-1975 to mid 1980, totalling 

303 cases, were identified. After exclusions, a group of 183 men (136 living 

and 47 dead) were studied. Controls were a sample of males, matched for 

ethnicity, age, and vital status, identified from various local records. 

Information on demographics, occupational history, tobacco and alcohol 

consumption and diet was collected by interview of participants or close 

relatives. Employment in the construction industry was one of the occupations 

with a significantly increased RR, after adjustment for tobacco and alcohol 

consumption (RR 1.70, 95% CI 1.06-2.72). However, this group would have 

been exposed to a wide range of substances so it not possible to relate this 

finding to cement dust exposure. 

Flanders and Rothman (1982) studied 90 male cases of laryngeal cancer 

identified from a larger cancer study. The control group was 933 males 

identified with cancers of the haematopoietic system, prostate and rectum. 

Information on employment, tobacco consumption and demographics were 

obtained by interview. The alcohol and tobacco adjusted RR for employment 

in the construction industry was elevated at 1.5 (90% CI of 0.7-3.2). Among 

specific occupations, the RR for construction labourers was 1.3 (90% CI 0.4-

4.6). Again, this study provided no information specifically on cement dust as 

a risk factor. 

Flanders et al. (1984) studied 42 patients with newly diagnosed and 

histologically confirmed squamous laryngeal cancer attending a US group of 

hospitals between 1974 and 1979. Eighty-five control subjects, matched for 

age, gender, residence area, tobacco and alcohol, were selected from noncancer hospital patients. Workers who may have been exposed to cement 

were grouped into a very heterogenous group of ‘labourers or maintenance 

personnel’, which showed a significantly elevated estimated RR (4.6, 90% CI 

1.6-13.6). RRs for farmers and textile processors were also elevated. This 

small study provided no information on the potential for cement dust to cause 

cancer. 

Zagranski et al (1986) considered male patients attending two US hospitals 

with histologically confirmed laryngeal cancer first diagnosed between 1975 

and 1980 and who were alive at the time of the study (1980-1981). Controls 

were selected from male general surgical patients at the hospitals, matched 

for year of admission, decade of birth, county of residence, ethnicity and 

smoking status. After refusals and exclusions 92 cases and were 181 controls 

were studied. After adjustment for tobacco and alcohol consumption, the OR 

for working in the construction industry was less than 1. By occupation, the 

OR for ever working as a mason was elevated, at 2.2 (95% CI 0.9-5.8). 

Masons will have been exposed to dusts other than to just cement and a 

specific role for cement in causing laryngeal cancer cannot be identified from 

this study. 

41 
Rothman et al. (1980) reviewed the epidemiology literature for laryngeal 

cancer. The pre-1980 literature did not identify cement dust exposure as a risk 

factor, but it must be stated that occupational risk factors had not been 

adequately studied at this time. The review identified strong associations 

between both smoking and high alcohol consumption and laryngeal cancer. 

Overall, the earlier studies of risk factors for laryngeal cancer provide limited 

support for the existence of an association between working in the 

construction industry and laryngeal cancer, but provide no useful information 

about the risks associated with exposure to cement dust per se. 

3.4.2.4 Other recent mortality and cancer-related studies involving subjects 

with exposure to cement dust. 

These studies have only limited relevance to the assessment of the 

hazardous properties of Portland cement, and are only briefly considered. 

Potential occupational risk factors for multiple myeloma were investigated in 

Swedish construction workers (Lee et al. 2003). Incident cases of multiple 

myeloma for the period 1971-1999 among 365,000 members (about 80% of 

eligible workers) of a Swedish construction industry health care scheme were 

identified from the Swedish Cancer Registry. Occupational exposures were 

assessed in a semiquantitative manner on the basis of industry job codes. A 

total of 446 primary multiple myeloma cases were identified. The RR for 

cement exposure 1.0 (95% CI 0.76-1.28, 49 cases) after adjustment for age 

and body mass index, showing than cement was not a risk factor for multiple 

myeloma. 

Szadkowska (2001) conducted a nested case control study in pulp and paper 

workers. Three cases of lung cancer among persons with previous exposure 

to ‘cement, brick, sand, grindstone dust’ were identified, compared with none 

with such exposure among controls. No conclusions about the effects of 

cement dust can be drawn from this study. 

A retrospective cohort mortality was conducted in members of a US plasterers 

and cement masons trade union (Stern et al. 2001). All members dying during 

the periods 1972-1980 and 1984-1996 were included. There were 7811 

cement masons in the cohort, whose exposures were said to include cement 

dust, silica, asphalt and various solvents. Compared to the general population, 

cement masons had significantly higher mortality for cancer of the stomach 

(proportionate cancer mortality ratio 133, p<0.01) and for benign neoplasms 

(proportionate mortality ratio 132, p<0.01). Because of the wide range of 

occupational exposure experienced by the cement masons no conclusions 

about the effects of cement dust can be drawn. 

Krstev et al. (1998) conducted a death certificate based case control study of 

prostate cancer in 24 US States. The occupations of 60900 men with prostate 

cancer as a cause of death were identified and compared with age matched 

controls that had died of causes other than cancer. ‘Supervisor of brick 

42 
masons’ was one of over 70 occupations with a significantly increased odds 

ratio for prostate cancer. The extent of cement exposure experienced by this 

occupational group was not reported. 

Cancer in Illinois construction workers was investigated in a series of case 

control studies using subjects from the state Cancer Registry (Keller and 

Howe 1993). The risk of lung cancer was greater for construction workers 

than the general population of Illinois (OR 2.11, (95% CI 1.02-1.26), but this 

was thought to be due to higher tobacco consumption among the construction 

workers. Cement exposure was not identified as a risk factor for cancer. 

In a briefly reported study, the frequencies of sister chromatid exchanges 

(SCEs) in the lymphocytes of workers from an Indian Portland cement factory 

were measured (Fatima et al 1995). The exposed subjects were 59 nonsmokers, age range 24-54 years, who had been exposed to cement for 1-17 

years. The mean number of SCEs in the exposed workers was 8.98 per cell, 

compared with 3.5 among the controls. Within the exposed group the results 

were analysed according to whether the subjects had been exposed for 1-5, 

6-11, or 12-17 years. The frequency of SCEs appeared to be positively related 

to exposure duration, but this could have been due to age differences 

between the exposure groups, which were not taken account of in the 

analysis. This is a briefly reported investigation, with results that are without 

corroboration from other studies. Furthermore, the health significance of such 

an increased frequency of SCEs is not known. Therefore, no conclusions 

about the hazardous properties of cement dust can be drawn from this study. 

3.4.2.5 Summary of mortality and cancer studies involving workers with longterm exposure to cement dust 

HSE (1994) came to a position that there was no convincing evidence for an 

increased incidence of any site-specific cancer resulting from cement 

exposure, but acknowledged that the data available at that time were not 

consistently and reassuringly negative. Since the early 1990s, a number of 

relevant cancer cohort and case control studies have been published, 

conducted in groups exposed to cement either through employment in cement 

manufacturing or in the construction industry. These studies have identified 

associations between cement exposure and cancers at several specific sites: 

the stomach, lungs, colon, and head/neck. The support for a causal 

association of each of these cancers with Portland cement exposure is 

discussed with reference to strength of association, consistency, the presence 

of a dose-response relationship and biological plausibility. Evidence from 

experimental studies in animal or in vitro models, which can contribute to 

arguments for or against causality, are not available. 

Elevated SMRs for stomach cancer were seen in three out the four cohort 

studies conducted in cement manufacturing workers covered by HSE (1994). 

One cohort study in cement manufacturing workers included in this review, 

conducted in Lithuania, identified a dose-related trend towards an increased 

risk of stomach cancer, although the numbers of cases involved was very 

small. In contrast, cohort studies conducted in two Swedish Portland cement 

43 
plants and a Danish cement plant did not show increased risks for stomach 

cancer. There is a degree of consistency, since an association has been seen 

in four out of the six available cohort studies. The strength of association is 

moderate, with SMRs ranging from 1.19 to 1.77. In two studies there was 

evidence for a dose-response relationship, but the evidence was far from 

convincing because of the small number of cancer cases in each exposure 

subgroup. Overall, the case for causality is stronger than for the cancers at 

other sites, but the recent data does not change the picture of uncertainty 

presented in the early 1990s. 

An association between cement exposure and lung cancer was seen in a 

cohort study in Lithuanian cement manufacturing workers but this could have 

been due to smoking. A study in Icelandic cement masons showed an 

increased risk of lung cancer in comparison with the general population, 

reporting an SIR of 1.77 (95% CI 1.01-2.88) when allowing for a latency 

period of at least 30 years. Overall, evidence for causality is very weak 

because consistency across studies in different populations is lacking. 

Furthermore, the strength of the observed association was moderate, and 

dose-response information is not available. 

A comprehensive cohort investigation into cancer at two Swedish cement 

manufacturing plants showed an increased risk of right-sided colon cancer 

among workers with long-term cement exposure. However, the right side of 

the colon, or colon generally, was not identified as a cancer site associated 

with cement exposure in the other cohort studies. Again, evidence for 

causality must be considered to be weak because an association has not 

been observed in studies in different populations. However, the strength of 

association was greater than found for colon and lung cancers (SIR 4.3, 95% 

CI 1.7 - 8.9 for workers with more than 25 years exposure) and there was 

some evidence suggesting an increased risk with increasing duration of 

exposure. 

Concerning cancers of the head and neck, a series of recent population 

based case control studies conduced in Germany demonstrated an 

association between contact with cement through employment in construction 

and cancers at these sites, especially cancers of the pharynx and larynx. 

Earlier case control studies, conducted elsewhere, investigating the risk 

factors for laryngeal cancers provided limited evidence of an association 

between employment in the construction industry and an increased risk of 

laryngeal cancer, but these studies provided no useful information on the risks 

associated with exposure to cement per se. No information on the association 

between these types of cancer and cement can be derived from the cohort 

studies because head and neck cancers are rare and the cohort studies 

lacked the power to investigate such cancers. The strength of association 

between occupational contact with cement and cancer of the head and neck 

was generally moderate, with ORs or estimated RRs ranging from about 1.2 

to 2.4, although for one study the association was very strong as shown by an 

OR of 12.6. The association showed consistency within the series of studies 

conducted in southern Germany but only limited corroborative support is 

available in terms of consistency from studies of laryngeal cancer in other 

44 
populations. A dose-response relationship has not been demonstrated. 

Furthermore, the exposure assessments in these studies did not determine 

the quantitative nature of the cement exposure, or take account of other 

exposures that could be experienced by persons who have occupational 

contact with cement, so there is no clear picture of what the subjects were 

exposed to. Overall, evidence for a causal association between cement 

exposure and head and neck cancer is weak. 

Biological plausibility is considered as for all cancers together. As a highly 

alkaline substance, cement can cause irritation at sites of contact, such as the 

mouth, throat, and lungs. Persistent chronic irritation will cause repeated 

cycles of cell death, cell proliferation and other inflammatory responses. It is 

recognised that this process can be a step on the pathway to cancer. Thus it 

is biologically plausible that cement dust could have the potential to cause 

cancers at sites of contact. 

To conclude, a causal association between Portland cement exposure and 

cancer has not been established. Nevertheless, the findings of the recent 

studies reviewed in this document maintain the uncertainty concerning a 

possible risk of cancer raised by the earlier data reviewed by HSE (1994). 

45 
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Am J Epidemiol, 124, 67-76 

50 
Table 1 Summary of recent studies of non-malignant respiratory disease in workers with long-term exposure to 

Reference Country Study subjects Main investigations Main findingFell et al. 2003 Norway 119 cement factory workers, mainly 

retired. 50 blue collar controls, 

Respiratory questionnaire, spirometry. Current dust measurements. 

No differences workers and co

matched for age 

Mwaiselage et Tanzania 115 cement factory workers Spirometry, peak flow. Current dust Reduction in FVal. 2004 102 controls, with maintenance or measurements. correlation with 

office jobs at factory 

Laraqui Hossini Morocco 280 cement factory workers. 73 Respiratory questionnaire, spirometry. No Higher prevaleet al. 2002 controls with office jobs. exposure data, but dust levels high. spirometry defiMeo et al. 2002 Pakistan 50 cement factory workers. 50 Spirometry. No exposure information Reduction in FV

matched population controls. 

Al-Neaimi et al. UAE 75 cement factory workers. 134 Respiratory questionnaire, spirometry. Higher prevale2001 matched controls No exposure information. FVC, FEV1 and Noor et al. 2000 Malaysia 62 cement factory workers Respiratory questionnaire, spirometry. Higher prevale

70 controls from university. Current dust measurements. FVC, FEV1 and 

Mengesha et al. Ethiopia 53 cement factory workers. 211 Respiratory questionnaire, spirometry, Higher prevale1998 controls, non-dusty occupations peak flow. Current dust measurements. FEV1/FVC ratio 

exposure. 

Abuhaise et al. Jordan 348 cement factory workers, Respiratory questionnaire, spirometry Higher prevale1997 divided into 3 exposure groups Current dust measurements. exposure. SpiroChanrawanshi & India 365 cement factory workers. 45 Peak flow. No exposure information PEFR lower amPati 1996 controls shifts Yang et al. 1996 Taiwan 412 cement factory workers. 147 Respiratory questionnaire, spirometry Higher prevale

controls with office jobs Current dust measurements FVC, FEV1 and 

Yang et al. 1993 Taiwan 661 cement factory workers, Respiratory questionnaire, spirometry. Higher prevale

including 146 office workers Current dust measurements with highest ex

measurements

Abrons et al. USA 2640 cement factory workers. 1458 Radiography. Current dust measurements Increase preva1998 blue collar controls available abnormalities oAlvear-Galindo et al. 1999 

Mexico 425 cement factory workers Respiratory questionnaire. Semi-quant 

exposure assessment 

Prevalence of rwith highest ex

Abou-Taleb et UAE 304 cements factory workers Respiratory questionnaire Chronic cough al. 1995 workers, but no Laraqui et al Morocco 120 concrete factory workers. 120 Respiratory questionnaire Higher prevale2001 controls, civil servants concrete worke
Fell et al. (2003) is a retrospective cohort study, the remainder are cross-sectional studies 

Table 2: Summary of mortality and cancer morbidity studies in cement manufacturing workers or masons Reference Country Study subjects Main investigations Main findingJakobsson et al. 1993 

Sweden 2400 cement factory workers, 

at two plants 

Mortality and cancer morbidity, compared to 

Overall mortamortality for th

general population Risk of tumou

2.7, 95% CI 1

Jakobsson et al. 1994 

Sweden 1526 cement factory workers 

3965 blue collar workers 

Mortality and cancer morbidity, compared to 

Risk of tumoucement worke

8092 fishermen general population Cancer risks f

general popu

Vesbo et al. 1991 Denmark 546 cement factory workers Cancer morbidity No evidence 

856 unexposed controls cement worke

Smailyte et al. 2004 Lithuania 2498 cement factory workers Mortality and cancer 

morbidity, compared to general population 

Increased incworkers (SIR not taken acctrend towards cancer. 

Rafnsson et al. 1997 Iceland 1172 masons, using wet Cancer morbidity, compared Increased inc

concrete to finish buildings to general population (SIR 1.7, 95% 
Table 3 Summary of German case control studies for cancers of the oral cavity, pharynx and larynx 

Reference Location Study population Main findings Maier et al. 1991 Heidelberg, 

Gliessen 

200 male cases of cancer of the oral cavity, pharynx and larynx 800 male hospital patient controls, matched for age and size of home 

Elevated risk of cancer assoccement. Estimated RR 2.4 (95smoking and alcohol consump

Maier et al. 1992 Heidelberg 164 male cases of cancer of the larynx 

656 male hospital patient controls, matched for age and size of home 

Slightly elevated risk of canceexposure to cement. Estimateadjustment for smoking and a

Maier at al. 1994 Heidelberg 105 male cases of cancer of the pharynx 

656 male hospital patient controls, matched for age and size/location of home 

Elevated risk of cancer assoccement. Estimated RR 2.2 (95smoking and alcohol consump

Maier et al. 2002 Heidelberg 209 male cases of cancer of the oral cavity, 

pharynx and larynx 110 male hospital patient controls, matched for age, smoking and alcohol consumption 

Substantially elevated risk of cexposure to cement. The OR 

Dietz et al. 2004 Rhien-Neckar 

region 

257 cases of laryngeal cancer 769 controls from the general population, matched for age, gender and location of home 

Elevated risk of cancer assoccement. The OR was 1.2 (95% questionnaire or 2.0 (95% CI questionnaire, after adjustmenand socio-economic status.