Case Reports

In February 2005, the Healthy Start program

in the Collier County Health Department

(CCHD) in Florida identified three infants

with congenital anomalies who were born

within 8 weeks of one another and determined

that all three mothers had worked for the same

tomato grower (CCHD 2005). All three

women had worked on the grower’s Florida

farms in 2004 before transferring to its North

Carolina farms later that year (Table 1). In

August 2005, the North Carolina Department

of Health and Human Services (NCDHHS)

was notified of these births by the North

Carolina Department of Agricultural and

Consumer Services (NCDACS); this agency

had been notified by U.S. Environmental

Protection Agency (EPA) Region 4 in April

2005. The Centers for Disease Control and

Prevention (CDC) was alerted in September

2005, and with the assistance of state health

departments in Florida and North Carolina

collected case reports and pesticide exposure

histories. 

The CCHD searched the Healthy Start

program records for other birth defects cases

born between December 2004 and February

2005 and whose parents had the potential for

exposure to agricultural pesticides. No additional cases were identified. Medical records on

the three mothers and their infants were

obtained and reviewed by the CCHD and the

state health departments in Florida and North

Carolina. Charles A. Williams, a clinical

geneticist and professor of pediatrics and

genetics at the University of Florida, College of

Medicine (Gainesville, FL) reviewed case summaries obtained from the medical records and

provided the descriptions of the birth defects.

Exposure information was obtained from

NCDACS and the Florida Department of

Agriculture and Consumer Services (FLDACS),

which obtained pesticide application and

worker assignment records from the grower.

Additionally, each of the mothers and fathers

were interviewed in early 2005 by CCHD.

The mothers of case 1 and case 2 were also

interviewed in 2006 by NCDHHS. 

Because of the imprecision of the conception date, there is also imprecision in the calendar days that correspond to the maximal

sensitivity period for any given birth defect. As

the window of maximal sensitivity shifts, the

number of days involving pesticide exposure

may also change. Therefore, a range of days is

provided to reflect the minimum and maximum number of days of pesticide exposure

during the maximal sensitivity period. In

addition, because workers often worked in

several agricultural fields on a given day and

because the specific hours worked in each

field were not available, days of pesticide

exposure were categorized into “probable

days” and “possible days.” Probable days are

those days when the mother was scheduled to

work in a field that had a restricted entry

interval (REI) in effect the entire day.

Possible days consist of days when the mother

was scheduled to work in a field that had an

REI that was in effect for only a portion of

the day. On possible days, it is conceivable

that the mother did not work in the field

when the REI was in effect. This would be

the case if she worked only before the pesticide application occurred, or only after the

REI had expired. According to the Worker

Protection Standard (WPS), after the application of any pesticide on an agricultural establishment, the agricultural employer shall not

allow or direct any worker to enter or to

remain in the treated area before the REI has

expired, unless the worker is provided appropriate personal protective equipment (PPE)

(U.S. EPA 1997). There is no evidence that

PPE was provided to these mothers.

Information on the three cases is provided

in Tables 1 and 2. During the period of

organogenesis (approximately 14–59 days

after fertilization) when birth defects are most

likely to occur, all three mothers unknowingly worked in tomato fields that were under

an REI because the fields were recently

treated with pesticides, some of which have

Environmental Health Perspectives • VOLUME 115 | NUMBER 5 | May 2007 787

Research | Children’s Health

Address correspondence to G.M. Calvert, National

Institute for Occupational Safety and Health, 4676

Columbia Parkway, R-17, Cincinnati, OH 45226

USA. Telephone: (513) 841-4448. Fax: (513) 841-

4489. E-mail: jac6@CDC.GOV

The findings and conclusions in this report are

those of the authors and do not necessarily represent

the views of the Centers for Disease Control and

Prevention, the U.S. Environmental Protection

Agency, or each author’s state or county agency.

The authors declare they have no competing

financial interests.

Received 23 August 2006; accepted 21 February

2007.

Case Report: Three Farmworkers Who Gave Birth to Infants with Birth Defects

Closely Grouped in Time and Place—Florida and North Carolina, 2004–2005

Geoffrey M. Calvert,1 Walter A. Alarcon,1 Ann Chelminski,2 Mark S. Crowley,3 Rosanna Barrett,4 Adolfo Correa,5

Sheila Higgins,2 Hugo L. Leon,3 Jane Correia,4 Alan Becker,4 Ruth H. Allen,6 and Elizabeth Evans6

1Division of Surveillance, Hazard Evaluations, and Field Studies, National Institute for Occupational Safety and Health, Centers for

Disease Control and Prevention, Cincinnati, Ohio, USA; 2North Carolina Department of Health and Human Services, Raleigh, North

Carolina, USA; 3Collier County Health Department, Naples, Florida, USA; 4Florida Department of Health, Tallahassee, Florida, USA; 5National Center on Birth Defects and Developmental Disabilities, Centers for Disease Control and Prevention, Atlanta, Georgia, USA; 6Office of Pesticide Programs, U.S. Environmental Protection Agency, Washington, DC, USA

CONTEXT: There is little evidence linking adverse reproductive effects to exposure to specific pesticides

during pregnancy.

CASE PRESENTATION: In February 2005, three infants with congenital anomalies were identified in

Collier County, Florida, who were born within 8 weeks of one another and whose mothers worked

for the same tomato grower. The mothers worked on the grower’s Florida farms in 2004 before

transferring to its North Carolina farms. All three worked during the period of organogenesis in

fields recently treated with several pesticides. The Florida and North Carolina farms were inspected

by regulatory agencies, and in each state a large number of violations were identified and record

fines were levied.

DISCUSSION: Despite the suggestive evidence, a causal link could not be established between pesticide exposures and the birth defects in the three infants. Nonetheless, the prenatal pesticide exposures experienced by the mothers of the three infants is cause for concern. Farmworkers need

greater protections against pesticides. These include increased efforts to publicize and comply with

both the U.S. Environmental Protections Agency’s Worker Protection Standard and pesticide label

requirements, enhanced procedures to ensure pesticide applicator competency, and recommendations to growers to adopt work practices to reduce pesticide exposures.

RELEVANCE TO PROFESSIONAL PRACTICE: The findings from this report reinforce the need to reduce

pesticide exposures among farmworkers. In addition, they support the need for epidemiologic studies to examine the role of pesticide exposure in the etiology of congenital anomalies. 

KEY WORDS: congenital abnormalities, ectromelia, farmworkers, fungicides, Goldenhar Syndrome,

insecticides, micrognathism, pesticides, prevention and control, toxicity. Environ Health Perspect

115:787–791 (2007). doi:10.1289/ehp.9647 available via http://dx.doi.org/ [Online 21 February

2007]
been shown to be teratogenic when tested

individually in animals (Table 2). The REIs

for the chemicals listed in Table 2 ranged

from 12 to 48 hr.

Case 1: This infant was born with tetraamelia (absence of all four limbs) (Table 1).

The parents had no known birth defect risk

factors, and this was the mother’s first pregnancy. The period for limb development is

24–36 days after fertilization (Moore and

Persaud 2003). During this period, this

child’s mother worked in violation of the REI

for up to 4 days involving exposure to several

pesticides, including mancozeb (Table 2). 

Case 2: This infant was born with mild

Pierre Robin syndrome (micrognathia, high

arched palate, and mild persistent palatine

rugae). The father of this child has micrognathia. During gestational days (i.e., days

after fertilization) 14–57, this child’s mother

worked in violation of the REI for up to

8 days. On seven of these days, the pesticides

applied to the fields where the mother worked

included methamidophos. In addition, on

gestational days 7 and 10, the mother worked

in fields when an REI was possibly in effect

(mancozeb on both days, and abamectin and

methylpyrrolidone on day 7). The mother has

three other living children, none of whom are

known to have birth defects. This mother also

had one previous stillbirth but without obvious birth defects.

Case 3: This infant had multiple severe

malformations including cleft lip and palate,

imperforate anus, solitary kidney, vertebral

anomalies, dysplastic low-set ears, and

ambiguous genitalia. These findings are

quite reminiscent of a severe type of the

Goldenhar Syndrome (also referred to as

oculo–auriculo–vertebral sequence). Death

occurred at 3 days of age. During gestational

days 14–59, the mother worked in violation

of REIs for up to 10 days. On eight of these

days, the REI for methamidophos was in

effect on some of the fields where the mother

worked. Abamectin and methylpyrrolidone

were applied to some of the fields on two

other days, but the mother may have worked

in those fields before the applications were

made. The mother had two previous pregnancies. One pregnancy 3 years earlier involved a

malformed fetus and ended in miscarriage.

The mother could not recall her employment

or whether she had any toxic exposures during that pregnancy. The other previous pregnancy resulted in a normal child. 

None of the three mothers reported

tobacco or alcohol use, and none reported taking prescription, over-the-counter, or folk

medications. Maternal infections (e.g., syphilis,

rubella, cytomegalovirus, toxoplasmosis, and

herpes simplex virus) were ruled out as a cause

of the birth defects based on data available in

the medical records. All three mothers are

Mexican, have undocumented U.S. immigrant

status (i.e., they did not have a U.S. visa or

other immigration document), and sought prenatal care late in their pregnancies. All three

mothers reported morning sickness, but none

reported to the crew leader or grower that they

were acutely poisoned by pesticides while pregnant. Information on housing conditions during the pregnancies was unavailable. Each

child’s father was also employed as a farmworker for the same grower as the three mothers. Unfortunately, information on the three

fathers’ pesticide exposures was unavailable. 

Approximately 956 farmworkers were

employed at the Florida location and 500 at

the North Carolina location, 20% of whom

were women. The identity of the female farmworkers was not provided by the employer.

Thus, identification of other workers who

gave birth in 2004 or 2005 was not possible.

In 2005, the Florida and North Carolina

farms were inspected by FLDACS and

NCDACS, respectively. A large number of

violations were identified, and the grower

received among the largest fines ever imposed

by these enforcement agencies. Violations

identified by both agencies included failure to

prevent workers from entering pesticide-treated

fields before REI expiration, and failure of pesticide handlers to understand all pesticide label

requirements. NCDACS also documented failure to provide drinking water and water for

routine washing, whereas FLDACS did not

report on the availability of water. 

Discussion

Three farmworkers giving birth to infants with

birth defects within an 8-week period is cause

for concern. In Florida, approximately 3% of

live births have major birth defects. There is

evidence to suggest that the three observed

major birth defects exceed this expected rate.

To obtain the observed birth defects rate

among these farmworkers, one needs the

number of births for the period in question.

Unfortunately, there is no accurate information on the fertility rate among female farmworkers employed in Florida. However, based

on Collier County, Florida, Hispanic birth

rates (Florida Department of Health 2001;

U.S. Census Bureau 2001), it is estimated that

25 live births occur every year among the

191 female farmworkers employed in Florida

where the case mothers worked, or two live

births per month. Assuming the other three

births were normal (of the six expected live

births in the 12-week period that was investigated), these three infants with birth defects

would provide an incidence rate of 50% for

birth defects during the 12 weeks in question

among the female farmworkers employed in

Florida where the case mothers worked.

The etiology of most human birth defects

cases is unknown (Moore and Persaud 2003).

However, multifactorial interactions of genetic

and environmental factors are thought to be

responsible for 20–25% of birth defects,

genetic factors alone for 15–25%, and environmental agents alone for 7–10% (Moore and

Persaud 2003). Known risk factors include

chromosomal disorders, single gene mutations,

family history of birth defects, alcohol, some

medications, infections, tobacco, diabetes, and

lack of essential vitamins (e.g., folic acid)

(CDC 2006). Although animal toxicologic

studies provide evidence that high doses of

some pesticides can alter reproductive function

Calvert et al.

788 VOLUME 115 | NUMBER 5 | May 2007 • Environmental Health Perspectives

Table 1. Demographic and work history information on the infants with birth defects and their mothers.

Age of Days mother was Days mother was

mother at employed on grower’s employed on grower’s 

Estimated date time of infant’s Florida farms North Carolina farms 

Birth defects Date of birth of conceptiona Sex birth (years) after conceptionb after conceptionb

Case 1

Tetra-amelia 17 Dec 2004 3 Apr 2004 Male 19 0–14 16–182

Case 2

Micrognathia (underdeveloped jaw), high arched palate, and mild 4 Feb 2005 10 Apr 2004 Male 30 0–51 65–216

persistent palatine rugae

Case 3

Multiple malformations including cleft lip and palate, imperforate 6 Feb 2005 16 May 2004 Female 21 20–36 120–159

anus, solitary kidney, vertebral anomalies and very abnormal, 

dysplastic, low-set ears, and ambiguous genitalia, reminiscent 

of a severe type of Goldenhar syndrome

aThe conception date was calculated by adding 14 days to the onset date of the last menstrual period. Because the precise date of conception was unavailable, this date represents the

first date in a 2- week window that is thought to capture the precise conception date. bBased on the conception date provided in this table. 
and produce birth defects, few epidemiologic

studies have linked specific pesticide exposures

to reproductive toxicity in humans (Hanke and

Jurewicz 2004; Sever et al. 1997; Thulstrup

and Bonde 2006). 

There are serious concerns that during the

period of organogenesis all three mothers were

exposed early in pregnancy to pesticides shown

to be teratogenic in animals. Furthermore,

some of these exposures may have been high

because, according to the grower’s records, the

mothers worked in fields in which the REI had

not expired.

Mancozeb and its metabolite ethylenethiourea (ETU) have been shown to produce limb defects and cleft palate after high

oral doses were given to rats (Larsson et al.

1976). ETU has a biologic half-life of approximately 34 hr to 4 days (Kurttio and

Savolainen 1990). During the period of limb

development, the mother of case 1 may have

worked up to 4 days in fields in violation of

the REI for this fungicide. 

The mother of case 3 has evidence of

8 workdays (4 probable and 4 possible days)

of exposure to methamidophos, which has

evidence for teratogenicity in mice and rats

(Asmatullah and Aslam 1999; Hanafy et al.

1986). On at least three of the probable days,

this mother may have been exposed within

14 hr of the application. The REI for methamidophos is 48 hr. However, the U.S. EPA recommended in 2002 that the REI be increased

to 96 hr (U.S. EPA 2002). If the 96-hr REI

had been in effect in 2004, then this mother

would have had 10 days of working in violation of the REI [8 probable (days 22–24, 27,

30, 31, 33, 34), and 2 possible (days 26 and

27)]. Despite some animal evidence for teratogencity, we are aware of no authoritative

sources, including the U.S. EPA and the State

of California Environmental Protection

Agency, that have concluded that methamidophos is a teratogen (FLDACS 2005; Food

and Agriculture Organization/World Health

Organization 2002). 

The mother of case 2 had only one probable day working in violation of an REI during

the maximal sensitivity period, the fewest

number of the three mothers. However, this

mother had 8 days possibly involving work in

violation of an REI. The one probable day

and six of the possible days involved exposure

to methamidophos. We are unaware of animal

evidence for an association between the birth

defects found in case 2 and methamidophos

exposure; however, mancozeb and its metabolite ETU have been shown to produce abnormal shortening of the mandible (Larsson et al.

1976; Stula and Krauss 1977). Although the

potential mancozeb exposure for the mother

of case 2 was on days 7 and 10, the half-life of

this chemical and its metabolite suggests the

possibility of exposure during organogenesis.

Some may question whether this is a true

cluster because each of the babies had a different constellation of defects, and none of the

pesticides to which the mothers were probably exposed can be linked (in animal or

human studies) to all of the observed defects.

However, the differences in the birth defects

identified in this cluster may be attributed to

the differences in the conception dates, the

differences in the work histories of the three

mothers, and the large number of chemicals

used by the grower. There is evidence to suggest that each mother was exposed to pesticides during the maximal sensitivity period for

the organ system/structure that was affected.

As demonstrated in Table 2, all mothers

had the potential for exposure to pesticide

mixtures, and little is known about the teratogenicity of these mixtures. Animal toxicologic

studies are performed on individual chemicals,

and little is known about the reproductive

effects of exposure to mixtures of pesticides

that have different modes of action. However,

there is evidence in a mice model that pesticide mixtures can produce developmental

effects that would not be predicted or are

Farmworkers who gave birth to infants with birth defects

Environmental Health Perspectives • VOLUME 115 | NUMBER 5 | May 2007 789

Table 2. Days worked during the first 2 months of pregnancy in violation of an REI and pesticides for which an REI was in effect.

Estimated period 

of organogenesis Total days Pesticides mother was

for specific worked in potentially exposed Specific gestational days worked in

birth defect (days specified period of to during maximal violation of an REI to the given pesticideb Some teratogenic findings from 

Mother after fertilization)a organogenesisb sensitivity period Specific probable daysc Specific possible daysd testing of pesticide in animalse

Case 1 24–36 2–6 Mancozeb Days 19, 32, 37, 39, 41 Limb reduction defects, cleft palate, 

and brachygnathia

Copper hydroxide Days 19, 32, 37, 39, 41 No data found

Bacillus thuringiensis Days 19, 32, 37, 41 No data found

Spinosad Days 31, 39 No teratogenicity identified

Azadirachtin Day 41 No data found

Bacillus subtilis Day 41 No data found

Case 2 14–57 21–27 Mancozeb Days 7, 10 Limb reduction defects, cleft palate 

and brachygnathia

Methamidophos Days 10, 28 Days 7, 26, 27, 38, 39, 40 Anotia, anencephaly, paddle-shaped 

limbs, microphthalmia

Abamectin Day 7 Cleft palate

Methylpyrrolidonef Day 7 Cleft palate 

Copper hydroxide Days 7, 10, 45 No data found

Fenpropathrin Days 7, 10, 26, 27, 28, 38, 39 No teratogenicity identified

Chlorothalonil Days 10, 26, 27, 28, 38, 39 No teratogenicity identified

Esfenvalerate Day 7 No teratogenicity identified

Methomyl Day 45 No teratogenicity identified

Case 3 14–59 5–11 Methamidophos Days 22, 30, 33, 34 Days 23, 25, 26, 31 Anotia, anencephaly, paddle-shaped 

limbs, microphthalmia

Abamectin Days 24, 29 Cleft palate

Methylpyrrolidonef Days 24, 29 Cleft palate

Fenpropathrin Days 30, 33 Days 22, 24 No teratogenicity identified

Hydrogen dioxide Day 23 No data found

Chlorothalonil Day 24 No teratogenicity identified

aBased on Moore and Persaud (2003). bBecause of the imprecision of the conception date, there is also imprecision in the calendar days that correspond to the maximal sensitivity

period. As the window of maximal sensitivity shifts, the number of qualifying days may change. The numbers provided reflect the range of qualifying days. cProbable days are those days

when the worker was scheduled to work in a field that had an REI that was in effect the entire day. dPossible days consist of days when the mother worked in a field that had an REI that

was in effect for only a portion of the day. On possible days, it is conceivable that the mother did not work in the field when the REI was in effect. This would be the case if she worked

only before the application occurred, or only after the REI had expired. Detailed information on the hours worked in specific fields was not available. eAs summarized in FLDACS (2005).

“No data found” = no studies that explored the teratogenicity of the compound were identified by FLDACS. “No teratogenicity identified” = when teratogenicity studies were conducted

and all were found to be negative. f

This chemical is included in the same pesticide product as abamectin but is not an active ingredient (i.e., it is considered an inert ingredient). 
Calvert et al.

790 VOLUME 115 | NUMBER 5 | May 2007 • Environmental Health Perspectives

more severe than predicted based on the

known toxicology of each individual pesticide

(Cory-Slechta 2005). 

All three mothers had the potential for

three routes of exposure: dermal, inhalation,

and oral. It is not possible to determine which

route most contributed to their internal dose

of pesticides. Many host, agent, and environmental factors affect the relationship between

the potential exposure and the resulting

absorbed dose (Solomon et al. 2005). When

the route of exposure is dermal, the internal

dose can be modified by many factors including the area and location of the skin exposed,

the amount of pesticide residue on the foliage

that can be dislodged, the presence of skin

damage, environmental temperature and

humidity, the presence of other compounds

on the skin, and the inherent transcutaneous

absorption properties of the pesticide

(Boeniger 2003). As for the inhalational route

of exposure, the internal dose can be modified

by the respiratory rate, which increases with

physical exertion, and the vapor pressure of

the pesticide. Finally, oral exposure can take

place if pesticide-contaminated food or drink

was consumed. This could occur if the mothers did not wash their hands before eating.

Among the citations issued by NCDACS was

a lack of hand-washing facilities at one farm

site where the women worked, and failure to

provide adequate amounts of drinking water

(Chelminski and Higgins 2006). In addition,

there is no evidence that the women were

provided with PPE, such as chemically resistant gloves and clothing to reduce dermal

exposure to pesticides.

There is no evidence that the three mothers described in this report experienced toxicity associated with their gestational pesticide

exposures. Although many teratogenic exposures also produce adverse effects on the

mother, there are exceptions. For example, a

study in which rats were administered a dermal dose of 50 mg/kg body weight/day of

ETU on days 12 and 13 of gestation produced malformations in all fetuses (including

encephalocele, short mandible, and missing

leg bones) but produced no substantial acute

effects on the dams (FLDACS 2005; Stula

and Krauss 1977). Another study in which

pregnant mice were given a single intrapertioneal injection of 80 mg/kg body weight of

chlorpyrifos (an organophosphate pesticide)

produced a significantly increased rate of malformed fetuses, including cleft palate and

absent thoracic vertebrae, compared to a control group exposed only to the vehicle, but the

pesticide produced no overt signs of maternal

toxicity (Tian et al. 2005). The dose of 80

mg/kg body weight of chlorpyrifos was chosen by the investigators because it was “below

doses that may cause significant inhibition of

cholinesterase activity” (Tian et al. 2005).

Cholinesterase inhibition is one of the most

sensitive toxic end points produced by

organophosphate pesticides (U.S. EPA

2006a). In addition, newborn children, and

perhaps fetuses, may be substantially more

susceptible to toxicity from pesticide exposure

compared to their mothers. For example,

plasma paraoxonase 1, an enzyme involved in

organophosphate detoxification, has recently

been shown to have both significantly lower

concentrations and significantly lower enzyme

detoxification activity in newborn infants

compared with their mothers, suggesting

increased susceptibility to organophosphate

toxicity among infants (Furlong et al. 2006;

Holland et al. 2006). With increased susceptibility, pesticide exposure may produce toxicity in the fetus while sparing the mother. 

Although evidence of acute pesticide poisoning among the three mothers is absent,

limited contemporaneous means were available to identify maternal pesticide toxicity.

Their undocumented immigrant status and

lack of health insurance limited their access to

medical care, as evidenced by the fact that

none of the three mothers received prenatal

care before the second trimester of pregnancy.

Furthermore, because the mothers may not

have known the symptoms associated with

pesticide toxicity, any such symptoms may

have been attributed to their pregnancy. All

three mothers reported morning sickness,

whose symptoms such as nausea and headache can resemble pesticide poisoning. 

There are several limitations with this

report. Because a complete cohort of the

grower’s employees could not be ascertained, it

was not possible to fully characterize their birth

defect risk. Because some birth defects are not

diagnosed for months to years after birth, it is

possible that additional undetected birth

defects exist among this farmworker cohort.

Although the presence of family history for

case 2 and the multiple, complex defects for

case 3 suggest the likelihood of a genetic etiology, it was not possible to conduct evaluations

of genetic causes. Information on pesticide

exposure was based on company records,

which may be inaccurate. Because pesticide

biomonitoring and environmental sampling

were not performed, the mothers’ exposures

could not be compared with the high doses

used in animal testing to produce developmental effects. In addition, all three mothers

received late prenatal care, and nutritional supplementation was not begun until after prenatal care commenced. Moreover, previous

reports of clusters of birth defects and presumed occupational exposures have, in light of

additional evidence, been found to be more

complicated problems or related to factors not

measured in the original studies (Missmer et al.

2006; Williams et al. 2002). Finally, information was unavailable on paternal occupational

pesticide exposures, although each child’s

father was also employed as a farmworker for

the same grower as the three mothers. Given

these limitations, the small number of cases,

the lack of an epidemiologic study involving

the grower’s cohort of exposed workers in

Florida and North Carolina, and no known

published epidemiologic studies of birth

defects and the pesticides of concern, the evidence available is inadequate to establish a

causal relationship with pesticide exposures.

Despite these limitations and the lack of a

clear etiology for the observed birth defects,

the case series raises serious concerns that

some farmworkers may experience unsafe pesticide exposures when pesticide label directions are not followed (U.S. EPA 1996).

These exposures reinforce the importance of

compliance with and enforcement of existing

pesticide regulations, including the WPS

and the Occupational Safety and Health

Administration’s Field Sanitation Standard

(1987). North Carolina and Florida have

approximately 54,000 and 44,000 farms

respectively (U.S. Department of Agriculture

2004), but only 23 and 20 farm inspectors to

enforce pesticide regulations (U.S. EPA

2006b). Strengthened procedures to certify

the competency of private pesticide applicators

for safe pesticide applications also may be

needed. In addition, work practices should be

implemented to reduce pesticide exposures. In

late 2005, the grower voluntarily agreed to

cease use of mancozeb, methamidophos, and

abamectin. It is important that appropriate

training be provided to farmworkers, including

information on the adverse effects associated

with occupational pesticide exposures. In addition, because all three mothers sought prenatal

care only late into their pregnancy, improved

access to medical care among farmworkers

appears needed. Finally, improved surveillance

programs for pesticide-related illness and birth

defects are needed, as well as increased capacity

to investigate future birth defects clusters with

suspected workplace etiologies.

REFERENCES

Asmatullah, Aslam T. 1999. Toxicity of methamidophos in pregnant mice and developing fetuses. Punjab Univ J Zool

14:141–151.

Boeniger MF. 2003. The significance of skin exposure. Ann

Occup Hyg 47: 591–593. 

CCHD. 2005. Collier County Health Department Investigation

into the Occurrence of Congenital Malformations in

Immokalee, Collier County, Florida, 2005. Naples, FL:Collier

County Health Department, Florida Department of Health.

Available: http://www.doh.state.fl.us/chdcollier/pdf/

Birth_Defects_Report.pdf [accessed 18 January 2007].

CDC. 2006. Recommendations to improve preconception health

and health care—United States: a report of the

CDC/ATSDR Preconception Care Work Group and the

Select Panel on Preconception Care. MMWR 55(RR6):1–23. Available: http://www.cdc.gov/mmwr/preview/

mmwrhtml/rr5506a1.htm [accessed 18 January 2007].

Chelminski AN, Higgins S. 2006. Assessment of Maternal

Occupational Pesticide Exposures during Pregnancy and
Three Children with Birth Defects: North Carolina, 2004.

Raleigh, NC:North Carolina Department of Health and

Human Services. Available: http://www.epi.state.nc.us/epi/

oii/Agmartreleasereport.pdf [accessed 18 January 2007].

Cory-Slechta DA. 2005. Studying toxicants as single chemicals:

does this strategy adequately identify neurotoxic risk?

Neurotoxicology 26:491–510.

FDOH. 2001. Florida 2000 Vital Statistics Annual Report.

Tallahassee, FL:Florida Department of Health. Available:

http://www.flpublichealth.com/VSBOOK/VSBOOK.aspx#

[accessed 18 January 2007].

FLDACS. 2005. Teratogenic Potential of Pesticides Associated

with Florida Ag-Mart Farmworker Investigation.

Tallahassee, FL:Florida Department of Agriculture and

Consumer Services.

Food and Agriculture Organization/World Health Organization.

2002. Methamidophos. Pesticide Residues in Food-2002-

Joint FAO/WHO Meeting on Pesticide Residues. Available:

http://www.inchem.org/documents/jmpr/jmpmono/

2002pr10.htm#1.2.5.2 [accessed 18 January 2007]. 

Furlong CE, Holland N, Richter RJ, Bradman A, Ho A, Eskenazi B.

2006. PON1 status of farmworker mothers and children as a

predictor of organophosphate sensitivity. Pharmacogenet

Genomics 16:183–190.

Hanafy MSM, Atta AH, Hashim MM. 1986. Studies on the teratogenic effects of tamaron (an organophosphorus pesticide). Vet Med J 34:357–363.

Hanke W, Jurewicz J. 2004. The risk of adverse reproductive

and developmental disorders due to occupational pesticide exposure: an overview of current epidemiological

evidence. Int J Occup Med Environ Health 17:223–243.

Holland N, Furlong C, Bastaki M, Richter R, Bradman A, Huen

K, et al. 2006. Paraoxonase polymorphisms, haplotypes,

and enzyme activity in Latino mothers and newborns.

Environ Health Perspect 114:985–991.

Kurttio P, Savolainen K. 1990. Ethylenethiourea in air and in

urine as an indicator of exposure to ethylenebisdithiocarbamate fungicides. Scand J Work Environ Health

16:203–207.

Larsson KS, Arnander C, Cekanova E, Kjellberg M. 1976.

Studies of teratogenic effects of dithiocarbamates maneb,

mancozeb, and propineb. Teratology 14:171–183.

Missmer SA, Suarez L, Felkner M, Wang E, Merrill AH Jr,

Rothman KJ, et al. 2006. Exposure to fumonisins and the

occurrence of neural tube defects along the Texas–Mexico

border. Environ Health Perspect 114:237–241.

Moore KL, Persaud TVN. 2003. The Developing Human:

Clinically Oriented Embryology. 7th ed. Philadelphia:W.B.

Saunders. 

Occupational Safety and Health Administration. 1987. Field

Sanitation Standard. 29 CFR 1928.110. Available: http://www.

osha.gov/pls/oshaweb/owadisp.show_document?p_table=

STANDARDS&p_id=10959 [accessed 18 January 2007].

Sever LE, Arbuckle TE, Sweeney A. 1997. Reproductive and

developmental effects of occupational pesticide exposure:

the epidemiologic evidence. Occup Med 12:305–325.

Solomon KR, Houghton D, Harris SA. 2005. Nonagricultural and

residential exposues to pesticides. Scand J Work Environ

Health 31 suppl 1:74–81.

Stula EF, Krauss WC. 1977. Embryotoxicity in rats and rabbits

from cutaneous application of amide-type solvents and

substituted ureas. Toxicol Appl Pharmacol 41:35–55.

Thulstrup AM, Bonde JP. 2006. Maternal occupational exposure and risk of specific birth defects. Occup Med (Lond)

56:532–543.

Tian Y, Ishikawa H, Yamaguchi T, Yamauchi T, Yokoyama K.

2005. Teratogenicity and developmental toxicity of chlorpyrifos. Maternal exposure during organogenesis in mice.

Reprod Toxicol 20:267–271.

U.S. Census Bureau. 2001. Census 2000 Summary File 1

(Collier County, FL). Washington DC:U.S. Census

Bureau. Available: http://factfinder.census.gov/servlet/

DatasetMainPageServlet?_program=DEC&_submenuId=

datasets_1&_lang=en&_ts= [accessed 18 January 2007].

U.S. Department of Agriculture. 2004. 2002 Census of

Agriculture. Washington DC:National Agricultural Statistics

Service, U.S. Department of Agriculture. Available: http://

www.nass.usda.gov/index.asp [accessed 18 January

2007].

U.S. EPA. 1996. Office of Prevention, Pesticides and Toxic

Substances Harmonized Test Guidelines. Occupational

and Residential Exposure Test Guidelines. Series 875.

Washington, DC:U.S. Environmental Protection Agency.

Available: http://www.epa.gov/opptsfrs/publications/

OPPTS_Harmonized/875_Occupational_and_Residential_

Exposure_Test_Guidelines/index.html [accessed

18 January 2007].

U.S. EPA. 1997. Worker Protection Standard. Washington DC:U.S.

Environmental Protection Agency. Available: http://

www.epa.gov/pesticides/safety/workers/PART170.htm

[accessed 18 January 2007].

U.S. EPA. 2002. Interim Reregistration Eligibility Decision for

Methamidophos. Case No. 0043. Washington DC:U.S.

Environmental Protection Agency. Available: http://

www.epa.gov/oppsrrd1/REDs/methamidophos_ired.pdf

[accessed 18 January 2007].

U.S. EPA. 2006a. Organophosphate pesticide (OP) cumulative

assessment—2006 Update. Washington DC:U.S.

Environmental Protection Agency. Available: http://www.

epa.gov/pesticides/cumulative/2006-op/index.htm

[accessed 18 January 2007].

U.S. EPA. 2006b. Certification and Training Plan and Annual

Report. Pullman, WA:Washington State University.

Available: http://134.121.87.199/candt/logon.cfm [accessed

18 January 2007].

Williams LJ, Honein MA, Rasmussen SA. 2002. Methods for a

public health response to birth defects clusters. Teratology

66:S50–S58. 

Farmworkers who gave birth to infants with birth defects

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