SUPPLEMENTAL REPORT TO THE CITY OF PHILADELPHIA 

DEPARTMENT OF PUBLIC HEALTH/ AIR MANAGEMENT SERVICES 

INCREASED TOXICITY and CARCINOGENICITY OF 

n-PROPYL BROMIDE (1-BROMOPROPANE) 

RELATIVE TO PERCHLOROETHYLENE 

Adam M. Finkel, Sc.D., CIH 

JUNE 2010 
2

1. INTRODUCTION: 

The city of Philadelphia has proposed to accelerate the federal (EPA) phase-down of 

perchloroethylene (“Perc”) in dry cleaning, due to health concerns for the residents 

(especially children) and workers in establishments co-located with cleaners. Although 

some co-commercial cleaners will likely stay with Perc and control exposures in colocated workplaces to the performance standard established in the new regulations (at or 

below 40 ppb), others will switch to different solvents, and all cleaners with co-located 

residences or “sensitive” facilities (schools, day care centers, hospitals, etc.) will either 

have to switch to another solvent or change their service to “drop mode” (for cleaning at 

another location). The Ad Hoc Subcommittee of the Air Pollution Control Board 

(APCB) was concerned about ensuring that alternative solvents whose use might increase 

on account of the regulations would be safer whenever possible, and certainly not more 

toxic than Perc: as its February 16, 2010 memo to the full APCB indicated, the 

Subcommittee wanted Air Management Services to “Promote switching to clearly safer 

substitutes and seek to prevent the use of other hazardous toxic substances as a 

substitute” (for Perc). Of the various “drain and drop” and other alternatives to Perc, 

some are clearly safer (e.g., wet cleaning, supercritical CO2,) some are probably less toxic 

but may raise concerns about flammability, but some are clearly more toxic. 

I was asked by AMS to summarize the current scientific information about the relative 

toxicity of Perc and one particular alternative—n-propyl bromide (“nPB,” also known as 

1-bromopropane). This report also discusses more generally the risk management issues 

that arise when a regulatory agency is faced with the likelihood that well-meaning 

controls on a particular substance will lead to a net increase in harm (Finkel 2007). 

Absent a more comprehensive regulatory structure, the obvious risk-increasing response 

to controls on Perc in dry cleaning will be for some cleaners to substitute nPB for Perc. 

nPB was relatively unknown in the U.S. 10 years ago, but since then has been 

aggressively marketed as an unregulated alternative first to methylene chloride (regulated 

by OSHA in 1997), and later to Perc following EPA’s announced phase-down in dry 

cleaning. For example, here is a very frank description from an industry website: 

http://www.textilecleaning.com/npropylb.htm. DrySolv is a newer 

alternative solvent that is available for drycleaners to get out from under 

perc and its related rules, regulations, taxes, continually rising cost 

and general bad publicity. (emphasis added) 

One of the major remaining manufacturers of nPB describes its advantages thus: 

http://www.envirotechint.com/products/dry-cleaning/details/drysolv. 

DrySolv is a patented dry cleaning solvent that is non-chlorinated, nonflammable, non-hazardous, and is vastly more environmentally 

responsible than PERC. It is a direct replacement for PERC and other 

cleaning chemicals in the dry cleaning industry that works in your existing 

PERC dry cleaning machine. Research has shown DrySolv to be superior 
3

to PERC in that it cleans better, and cleans faster. Because DrySolv is 

non-hazardous, costly issues such as environmental compliance and waste 

disposal of PERC are eliminated or significantly reduced. 

As this report will summarize, in my expert opinion, far from being “non hazardous,” 

nPB is a potent neurotoxin, and has recently been shown to be a potent animal 

carcinogen. To a reasonable degree of scientific certainty, equal exposures to nPB will 

harm more residents and workers than would exposures to Perc: both are harmful 

substances, but nPB is the more harmful of the two. 

Even worse than comparable levels of exposure to the two solvents (in theory) would be 

the potential for much greater exposures to nPB than to Perc in actual practice. nPB is 

more volatile than Perc (its vapor pressure is approximately 111 mm Hg at 25 C, whereas 

the vapor pressure of Perc is about 18.5 mm Hg), and so with equivalent equipment and 

controls, cleaners who use nPB would be expected to experience higher concentrations 

than if they used Perc. Indeed, data from a forthcoming journal article (Blando et al., 

2010) shows that in four New Jersey dry cleaners who recently switched from Perc to 

nPB, air concentrations of nPB were as high as 54 ppm as an eight-hour time-weighted 

average—Perc concentrations using similar (“third-generation”) equipment as the shops 

in New Jersey use tend to be only in the range of 1-5 ppm (OSHA 2006). Moreover, a 

regulation that only mentioned Perc would further tilt the playing field towards greater 

exposures to substitute materials, because the actual comparison would be of controlled 

exposures to Perc versus uncontrolled exposures to the substitute(s). Data from AMS 

(referenced in Section 5 of my January 2010 final report on Perc) shows that uncontrolled 

exposures to Perc in co-located facilities can approach 1 ppm (a reading of 864 ppb was 

documented with limited sampling); although interventions to control Perc emissions can 

reduce these concentrations to the 40 ppb performance standard or below, there would be 

no requirement or incentive for cleaners to undertake control measures if they were 

permitted to switch to nPB without such restrictions. So although this report will 

summarize the risk-increasing problem of comparable exposures to nPB versus Perc, in 

reality the untoward consequences of a regulation that does not anticipate and address 

adverse substitution would be much greater. 

2. SCIENTIFIC OVERVIEW: 

As this report will summarize, Perc at high levels (approx. 100 ppm) can cause moderate 

neurologic symptoms in exposed humans; at low levels (1 ppm and below) it can cause 

much less severe but still worrisome neurobehavioral symptoms. On the other hand, at 

high levels (roughly 50 ppm), nPB can cause severe neurological damage, but there are as 

yet no studies of neurobehavioral effects (present or absent) of nPB at low levels. 

Absence of evidence is not necessarily evidence of absence: in other words, we can’t 

assume that nPB won’t cause the same (or worse) neurobehavioral effects as Perc does at 

low levels. But presence of evidence trumps absence: in other words, we can be fairly 
4

confident that there is not a “Perc syndrome” of irreversible neuropathy at roughly 50-

100 ppm, because we have tested Perc at these levels and found different (less severe) 

human effects. 

Moreover, we can now compare the carcinogenic potency of the two solvents directly. 

The National Toxicology Program has now finished a set of lifetime cancer bioassays of 

nPB (NTP, 2009) to complement its 1986 studies of Perc. nPB is clearly somewhat more 

potent a carcinogen than Perc (see Section 2-C below). Although absence of evidence is 

not definitive here, I note that there are various interesting (though, in my opinion, not 

currently fully developed) theories as to why some of the Perc cancer results may be 

partially or wholly irrelevant to humans (see pp. 12-17 of my January 2010 report)—

there have been no such mechanistic attempts to explain away the variety of tumors 

found in the nPB bioassays.1 

Bitter experience with human diseases caused by low-molecular-weight brominated 

compounds (e.g., male sterility in Dow chemical plant workers caused by 

dibromochloropropane (“DBCP”), a compound closely related to nPB; neurological 

disease in workers exposed to the pesticide methyl bromide) suggests that brominated 

compounds are generally more toxic to humans than their chlorinated analogs. Several of 

these brominated compounds have since been banned nationally and internationally. This 

pattern of toxicity is consistent with the fact that the carbon-bromine bond is weaker than 

the C-Cl bond, and thus a brominated compound may more readily form an electrophilic 

intermediate that reacts with DNA, as compared to its chlorinated analog. Table 1 shows 

four pairs of compounds that differ only with respect to whether they contain bromine or 

chlorine atoms, showing that the brominated analog is up to 33 times more potent2

: 

 

 

1

 Note particularly that in the Perc bioassay, 22 percent of the test animals developed the sentinel tumor 

type (mononuclear cell leukemia) with NO exposure, whereas in the nPB bioassay the control rate (of lung 

tumors) was only 2 percent. Although I believe the MCL response for Perc is real and reliable (see my

January 2010 report), the enormous increase in lung tumors above control rates with nPB is even more 

compelling. 

2

 Note that although Perc is, of course, a chlorinated hydrocarbon, it does not appear in this table because 

there is essentially no toxicological or use information on “tetrabromoethylene,” which would be its direct 

brominated analog. 
5

TABLE 1 

DIRECT COMPARISON OF POTENCIES OF BROMINATED v. 

CHLORINATED ANALOGS 

Note: when comparing RfCs, the more potent toxicant is the one that has the lower value (a lower concentration 

corresponding to the same “likely to be without appreciable risk” outcome); when comparing cancer potency factors 

(“q1

* ” values), the more potent carcinogen has the higher value (more tumorigenicity per unit of exposure).

Substance Brominated Analog Chlorinated Analog Ratio Br:Cl 

 toxicity 

Ethylene di...X Ethylene dibromide: 

q1

*

= 6x10-4 (per ug/m3)

Ethylene dichloride: 

q1

*

= 2.6x10-5 (per ug/m3) 

23 : 1 

Methyl X Methyl bromide: 

RfC= 5x10-3 mg/m3

Methyl chloride: 

RfC= 9x10-2 mg/m3

18 : 1 

Vinyl X Vinyl bromide: 

RfC=3x10-3 mg/m3

Vinyl chloride: 

RfC=1x10-1 mg/m3

33 : 1 

Chloro-di(X,X) 

propane 

Dibromochloropropane 

(“DBCP”): 

RfC= 2x10-4

1,2,3-trichloropropane: 

RfC=3x10-4

1.5 : 1 

It is also important to note that various federal, state, and international expert bodies are 

gradually developing recommended or mandatory exposure limits for nPB that are 

stricter than the corresponding ones for Perc (Table 2). Each of these expert bodies 

develops recommended or binding exposure limits based on a careful analysis of all 

available toxicologic and epidemiologic data, applying a coherent set of assumptions and 

rules for interpreting such data. Note in particular that these lower limits for nPB were 

all set before the late 2009 release of the National Toxicology Program’s lifetime cancer 

bioassay on nPB, which if incorporated would tend to drive the recommended limit lower 

for nPB. 

TABLE 2 

NATIONAL AND INTERNATIONAL EXPOSURE LIMITS FOR 

nPB and PERC 

Type of Limit Limit for Perc Limit for nPB Ratio Perc : nPB 

ACGIH Threshold 

Limit Value® 

25 ppm 10 ppm 2.5 : 1 

California OSHA 

PEL 

25 ppm 5 ppm 5 : 1 

Worksafe British 

Columbia PEL 

25 ppm 10 ppm 2.5 : 1 
6

In addition to these decisions by expert bodies, individual companies have made 

decisions about nPB; in particular (Murphy 2001), a major multinational chemical 

company decided almost 10 years ago (long before the case reports of neurotoxicity and 

the cancer bioassay were available) that it would cease marketing nPB for solvent 

applications due to its toxicity. The document announcing that decision said in relevant 

part: 

“nPB is a part of a toxicologically suspect family in which several compounds 

have toxic properties identified in animals and confirmed in humans. In 1995 and 

then in 1996, we learned that isopropyl bromide, the structural isomer of nPB, had 

caused serious reproductive function problems in Korean and then in Chinese 

workers as well as blood effects following its use as a degreasing solvent... As 

the effects observed in animals for iPB have also been demonstrated in humans 

when used as solvent, the concerns expressed in 1997 about the potential effects 

of nPB in solvent applications are reinforced.” 

In addition, at least two other manufacturers have limited or eliminated the production of 

1-BP for solvent applications. Great Lakes Chemical no longer sells 1-BP solvent blends. 

Albemarle Corp. has stated that use of 1-BP in adhesive and other applications in which 

1-BP exposure cannot be controlled should be restricted or prohibited (NTP, 2003). 

3. DETAILED TOXICOLOGICAL COMPARISION 

The LC50 (the airborne concentration that kills 1⁄2 of all treated animals) for nPB is 

approximately 7,100 mg/m3

: the LC50 for Perc is approximately 35,000 mg/m3, 

suggesting that nPB is roughly 5 times more acutely toxic than Perc. However, more 

relevant to regulatory policy are comparisons of chronic exposures to lower levels of the 

two substances. 

A. Neurotoxicity: 

nPB, like Perc, can damage the central and peripheral nervous systems, but evidence to 

date strongly suggests that nPB is the more potent neurotoxin of the two. The severe 

effects of weakness and spasticity of the leg muscles in humans correspond closely to 

effects seen in laboratory animals exposed to nPB: 

• Ichihara et al. (2004) studied 27 female workers in an nPB production factory 

who were exposed to an average of 3 ppm (range 0.3 to 49 ppm). 15 of the 

workers showed diminution of the ability to sense vibration in the fingers and 

toes, including one worker (who lost this ability completely) whose exposure 

was 1.1 ppm. 

• Majersik et al. (2007) studied six workers who used a solvent containing 70% 

nPB to glue together foam pieces; their exposures ranged from 91 to 176 ppm, 
7

with durations of between 3 to 36 months. The workers experienced 

weakness and spasticity of the legs, chronic pain, memory loss, urinary 

incontinence, and daily headache while working with nPB. Even two years 

after cessation of exposure, some of the workers suffered from “markedly 

impaired cognitive function.” 

• Raymond and Ford (2007) studied eight workers exposed to nPB in glue used 

in a furniture factory in North Carolina. Average exposures were 

approximately 80 ppm. The workers developed unsteady, spastic gaits, loss of 

balance, and other neuromuscular signs and symptoms—in at least two of 

them, adverse effects (albeit milder in severity) were persisting eight years 

after having changed employment and presumed cessation of exposure. 

• The CDC (2008) reported on two workers with severe nPB neurotoxicity: (1) 

an electronics worker in Pennsylvania exposed to roughly 180 ppm developed 

ataxia (difficulty walking), which was persisting more than a year after 

cessation of exposure; and (2) a dry cleaner in New Jersey who used 

“DrySolv” (see above) developed tingling, numbness, muscular twitching, and 

visual disturbances—no information was presented as to whether these 

symptoms persisted after he began using a respirator at work (obviously, colocated residents and workers would/should not have the option of using 

protective equipment...). CDC wrote that this case “likely represents a 

sentinel case of neurologic toxicity in the dry cleaning industry, and 

additional cases could occur as dry cleaners switch from perchloroethylene 

use to 1-BP.” 

Although Perc clearly can cause dizziness and CNS depression at very high levels (above 

100 ppm), at levels comparable to those in these nPB case reports and studies, nothing 

like the “nPB syndrome” of gait disturbances and pain has been seen with Perc, over 

many decades of use. For example, although some of the earlier studies EPA references 

(Lauwerys et al. 1983; Seeber 1989—see p. 4-54 of EPA 2008) document effects of Perc 

at roughly 20 ppm that are more severe than the neurobehavioral effects used to set the 

RfC (e.g., lightheadedness), these studies revealed “no fine motor function deficits”—

whereas slightly higher levels of nPB have caused irreversible effects on the gross motor 

function of exposed workers. 

In summary, at comparable levels (roughly 50-100 ppm), Perc produces moderate 

neurotoxic effects (diminished sensitivity to vibration; reduced nerve conduction 

velocities), but nPB can produce severe and apparently irreversible neuropathy, affecting 

gait and cognition. The neurobehavioral effects of Perc at much lower levels (1 ppm and 

less), such as decreased reaction time and decreased color vision sensitivity, have not 

been looked for (yet) with nPB—but whether or not they are shown to occur, the clear 

danger of nPB at higher exposures makes controlling nPB levels an important addition to 

the Philadelphia regulation governing the use of Perc in co-located dry cleaners. 
8

B. Reproductive Toxicity: 

There is much more concern about nPB than about Perc along this dimension. In 

particular, most of the workforce (64 percent of the females and 75 percent of the males) 

of an entire factory in Korea was sterilized due to exposure to roughly 12 ppm of 2-BP 

(isopropyl bromide).3 2-BP is a different substance than nPB, but its very high toxicity is 

relevant here because it is an inevitable contaminant of the commercial manufacture of 

nPB.4 California has listed nPB as “known to cause developmental toxicity in both 

females and males” since 2004—it does not list Perc as a developmental toxicant. 

The NTP Center for the Evaluation of Risks to Human Reproduction (CERHR) evaluated 

the potential for 1-bromopropane (nPB) to produce adverse reproductive and 

developmental effects in humans (NTP, 2003). CERHR concluded that there was 

convincing evidence for reproductive and developmental toxicity in experimental 

animals. Evidence in humans was limited, but in the monograph, note was made of a new 

case that was not available to the expert panel indicating positive findings in women 

(altered menstruation) occupationally exposed to 1-bromopropane. The overall NTP 

conclusion was that “there is serious concern for reproductive and developmental effects 

of 1-bromopropane at the upper end of the human occupational exposure range (18 to 381 

ppm).” “Serious concern” is the highest level of NTP conclusion regarding the 

possibilities that human development and reproduction might be adversely affected. 

C. Carcinogenicity: 

The U.S. National Toxicology Program began testing nPB in roughly 2001, and released 

an extensive report (NTP 2009) in late 2009. As with other brominated alkanes of low 

molecular weight tested previously, nPB showed “clear evidence” (according to NTP) of 

carcinogenicity in multiple animal bioassays. NTP noted that nPB caused rare tumors of 

the large intestine in both male and female F344 rats, and tumors of the lung and 

 

3

 Note especially that the workers in the North Carolina furniture factory (Raymond and Ford 2007) were

found to have been exposed to 2-BP at levels up to 0.68 ppm—this is less than 1/10 the amount that caused 

severe reproductive toxicity in Korea, but it shows that commercial formulations containing nPB in the

U.S. may well have significant trace amounts of 2-BP. It makes sense that 2-BP levels would be about 

1/200 that of 1-BP in air, since (Shubkin and Liimatta 1998) one of the patent holders recommends that

when producing nPB, “the isopropyl bromide content should be kept low—for example, within the range of

from about 0.01 to 0.5 %.” The higher figure (0.5%) corresponds to 1 part in 200. 

 

4

 Note that because of trade secret concerns, we also don’t know much about the stabilizers added to nPB. 

Apparently, while commercial Perc formulations used in dry cleaning only require about 1% stabilizer 

content, nPB products require about 6-7%. Although depending on the identities of the stabilizers, this may 

not be a public health issue, even with stabilizers added nPB is more corrosive to metal than Perc, and thus 

may be harder on dry cleaning equipment (see, e.g., the IRTA 2009 article which interviews a dry cleaner 

in California who claims that switching to nPB created a cloud of acid that “ate a hole in his boiler,

completely destroyed the PERC machine and also corroded a laundry dryer in the facility beyond repair”).
9

bronchus of female mice—it also noted that tumors of the skin, pleura (mesothelioma), 

and pancreas in rats may have been related to nPB exposure. 

EPA has not yet analyzed the nPB bioassay data to calculate a cancer potency factor 

(CPF) that could be compared to the CPF for Perc. As described in detail in my January 

2010 report, the EPA CPF for Perc underwent an extensive set of modifications to 

account for the different pharmacokinetics of absorption, partition, and excretion in 

rodents versus humans—no such adjustment can be made for nPB because no PBPK 

model currently exists for that compound. Nevertheless, it is routine and instructive to 

compare the CPFs on an equal footing (that is, with no PBPK modifications). I estimated 

the dose-response curves for both substances using a computer program (“MSTAGE87,” 

courtesy Edmund Crouch, Ph.D.) that emulates EPA’s linearized multistage program, and 

then, following EPA practice, calculated the upper 95th percentile confidence limit on the 

linear term of the dose-response function, which EPA terms “q1

*

,” or the CPF. 

The most sensitive sex/strain/site combination for Perc carcinogenesis appears to be the 

mononuclear cell leukemia response in male rats (see January report). In that 

experiment, Perc caused 14 cancers at 50 ppm (all Perc and nPB results are out of 50 

animals per dose group), 22 at 200 ppm, and 27 at 600 ppm—at no exposure (control 

group), 11 cases of MCL were noted. In the recent bioassay of nPB, there was 1 

lung/bronchus tumor at no exposure, 9 at 62.5 ppm, 8 at 125 ppm, and 14 at 250 ppm. 

Note that nPB clearly caused many more excess tumors at lower doses as compared to 

Perc.

The dose-response software yielded a q1

* value of 1.95x10-3 (per ppm) for nPB, as 

compared to a value of 1.46x10-3 for Perc. By this comparison (which, again, cannot take 

PBPK into account, which could result in higher or lower relative potency for nPB 

compared to Perc), nPB is roughly 34% more potent per unit of exposure a carcinogen 

than Perc is.5

The chart below shows the two bioassays (in the black-and-white version of this 

document, the Perc data points are diamond-shaped and the nPB data points are squares; 

the upper-bound linear slope estimate is a thicker line for nPB and a thinner line for 

Perc). In both cases, the y-values represent the number of tumor-bearing animals above

the number in the control group. Note that the upper confidence limit on the low-dose 

slope is larger (steeper) for nPB than it is for Perc. 

 

5

 Note that the recent National Academy of Sciences committee (NAS 2010) that looked carefully at the 

carcinogenicity data for Perc was divided about the confidence with which we should rely on the rat 

leukemia response, because of a possible species-specific mechanism of action. Although I agree with 

those on the NAS committee who regard the leukemia data as relevant, if one did compute Perc’s cancer 

potency based on the kidney tumor data, the q1

* value would instead be 3.8x10-4, which would make nPB 

more than five times more potent a carcinogen than Perc. 
10

0

5

10

15

20

25

30

0 50 100 150 200 250

dose (ppm)

# tumors above control response

observed perc tumor data

observed nPB tumor data

low-dose slope of Perc

low-dose slope of nPB

4. POLICY OVERVIEW: 

Risk-risk tradeoffs are real and compelling—although sometimes there is too much 

uncertainty about the eventual behavioral response to regulation (Finkel 2007) for 

government to regard a purported tradeoff as legitimate, there clearly are cases where as 

one substance is more tightly controlled, a more toxic substitute will almost certainly 

replace it, causing a net increase rather than a decrease in risk. This reflects lack of good 

planning by government; the “regulatory czars” under both the Bush and Obama 

administrations (Sunstein, 1996; Graham and Wiener 1995) have each written 

extensively about the need for statutory change so that agencies will be forced to consider 

the risk-increasing consequences of their regulations. 

There are three basic responses to a valid concern that regulating X will cause substance 

Y to be used, with net risk-increasing results: (1) regulate X and ignore the consequences; 

(2) forego regulating X entirely; or (3) regulate both X and Y. The first response is 

dereliction of duty, and the second is cringing in the face of a more complicated problem; 

the third course of action generally makes the most sense. 

Examples already exist of federal and state agencies causing increased net risk by 

regulating particular solvents without considering that users will seek unregulated 

substitutes, especially whenever one solvent can be “dropped in” to replace another with 

little or no retrofitting. For example, California cracked down on Perc use as a brakecleaning solvent in auto repair shops in the late 1990s; since then, case reports have 

arisen (CDC 2001) connecting serious neurological damage in auto repair workers whose 

shops switched to n-hexane. 

The momentum is clear that regulatory agencies should and will think more seriously 

about risk-risk tradeoffs. It is of course best to do so before it is too late. After the 
11

“genie is out of the bottle,” irreversible harm to human health or the environment may 

have occurred, but it is also important to emphasize that irreversible expense may also 

have been incurred: dry cleaners deserve the regulatory agency’s best current judgment 

about which substance(s) should not be used as substitutes before they are led to make 

investments that later prove unwise. Sometimes the risks of current materials and their 

substitutes confront society with a true dilemma—but this is not such a case—there are 

ways to clean clothes safely without using a solvent that is even more toxic than Perc. 

5. CONCLUSIONS 

nPB is a potent neurotoxin, and has recently been shown to be a potent animal 

carcinogen. As a result of my scientific analysis, I recommend that Philadelphia add a 

provision to its draft regulation forbidding dry cleaners to substitute the more toxic 

alternative nPB for perchloroethylene (“Perc”). This is a laudable and forward-thinking 

improvement to the federal (EPA) dry cleaning rule, which will, in my opinion, increase 

risks to workers and nearby residents by encouraging the substitution of the (federally) 

unregulated nPB for Perc in locales other than Philadelphia.6 To a reasonable degree of 

scientific certainty, exposures to nPB will harm more residents and workers than would 

exposures to Perc: both are harmful substances, with nPB the more harmful of the two. 

In addition to its plans to provide outreach and education to dry cleaners about ways to 

meet or go beyond the 40 ppb performance standard in co-commercial facilities that wish 

to continue to use Perc, I applaud the City’s intention to provide informational materials 

about the benefits of less toxic substitutes for Perc in dry cleaning. 

 

6

 Note that in the substitution of hexane for Perc, one could reasonably argue that while both substances are 

neurotoxic, only Perc is a probable carcinogen, and so the tradeoff was not necessarily an unfavorable one 

for workers. As this report will summarize, however, both Perc and nPB are animal carcinogens, and so no 

such “silver lining” can be invoked in this case. Switching to nPB is likely to increase both cancer and 

non-cancer risks. 
12

6. REFERENCES 

Blando, James, D., Donald P. Schill, Mary P. De La Cruz, Lin Zhang, and Junfeng Zhang 

(2010). “Preliminary Study of Propyl Bromide Exposure among New Jersey Dry 

Cleaners as a Result of a Pending Ban on Perchloroethylene.” Journal of the Air and 

Waste Management Association, forthcoming August 2010 (Vol. 60, No. 8), 8 pp. 

CDC, Morbidity and Mortality Weekly Report (MMWR), November 16, 2001, (Vol. 50, 

No. 45), pp. 1011-3. “n-Hexane-Related Peripheral Neuropathy Among Automotive 

Technicians—California, 1999-2000.”

CDC, Morbidity and Mortality Weekly Report (MMWR), Dec. 5, 2008, (Vol. 57, No. 48), 

pp. 1300-2. “Neurologic Illness Associated with Occupational Exposure to the 

Solvent 1-Bromopropane —New Jersey and Pennsylvania, 2007-2008.” 

Environmental Protection Agency (2008). Toxicological Review of 

Tetrachloroethylene, In Support of Summary Information on the Integrated Risk 

Information System. Report No. EPA/635/R-08/011A, June 2008, 556 pp. 

Finkel, A. M. (2007). “Distinguishing Legitimate Risk-Risk Tradeoffs from Straw 

Men.” Presentation at the Annual Meeting of the Society for Risk Analysis, San 

Antonio, TX, Dec. 11. 

Graham, J.D. and Jonathan Wiener, eds, Risk Versus Risk: Tradeoffs in Protecting 

Health and the Environment. Harvard Univ. Press, 1995. 

Ichihara, Gaku, and 14 others (2004). “Neurologic Abnormalities in Workers of a 1-

Bromopropane Factory.” Environmental Health Perspectives, 112(13): 1319-1325. 

Institute for Research and Technical Assistance (IRTA) (2009). “n-Propyl Bromide 

Destroys Equipment in Dry Cleaning Plant,” The Alternative (IRTA Newsletter): 

18(3): pp. 1, 6, 7, Summer 2009. 

Koh, J.M., et al. (1997). “Primary Ovarian Failure Caused by a Solvent Containing 2-

Bromopropane.” European Journal of Endocrinology, 138(5): 554-6. 

Majersik, Jennifer J. et al. (2007). “Severe Neurotoxicity Associated with Exposure to 

the Solvent 1-Bromopropane (n-propyl bromide),” Clinical Toxicology, 45: 270-6. 

Murphy, Sandi (2001). E-mail from ATOFINA (multinational chemical company, 

now known as Total/Arkema) to Dr. Michael Shelby, Director of the NIEHS Center 

for the Evaluation of Risks to Human Reproduction. Sent Sept. 27, 2001; 3 pp. 

including attachment; complete document available at 

http://cerhr.niehs.nih.gov/chemicals/bromopropanes/pubcomm/Atofina.pdf. 
13

National Academy of Sciences (2010). Review of the Environmental Protection 

Agency’s Draft IRIS Assessment of Tetrachloroethylene, prepublication copy, 140 pp. 

National Toxicology Program (2003). NTP/CERHR Monograph on the Potential 

Human Reproductive and Developmental Effects of 1-Bromopropane, October 2003, 

NIH Publication No. 04-4479, 88 pp. 

National Toxicology Program (2009). NTP Technical Report on the Toxicology and 

Carcinogenesis of Studies of 1-Bromopropane in F344/N Rats and B6C3F1 Mice. NTP 

TR-564, November 19, 223 pp. 

Occupational Safety and Health Administration (2006). Reducing Worker Exposure 

to Perchloroethylene (PERC) in Dry Cleaning. Report No. OSHA 3253-05N, 28 pp. 

Rascoff, Samuel and Richard Revesz (2002). “The Biases of Risk Tradeoff Analysis: 

Towards Parity in Environmental and Health-and-Safety Regulation.” Univ. of 

Chicago Law Review, 69: 1763-1836. 

Raymond, Lawrence W. and Marsha D. Ford (2007). “Severe Illness in Furniture 

Makers Using a New Glue: 1-Bromopropane Toxicity Confounded by Arsenic,”

Journal of Occupational and Environmental Medicine, 49(9): 1009-1019. 

Shubkin, Ronald L. and Eric W. Liimatta (1998). “N-propyl Bromide Based Cleaning 

Solvent and Ionic Residue Removal Process.” U.S. Patent No. 5,792, 277, granted 

August 11, 1998. 

Sunstein, Cass (1996). “Health-Health Tradeoffs,” Univ. of Chicago Law Review, 63: 

1533-71. 

Wiener, Jonathan (1998). “Managing the Iatrogenic Risks of Risk Management.” 

RISK: Health, Safety & Environment 9: 39-82.