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Eliminating Environmental Tobacco Smoke In The Workplace

The National Institute for Occupational Safety and Health (NIOSH) has determined that environmental tobacco smoke (ETS) is potentially carcinogenic to occupationally exposed workers. In 1964, the Surgeon General issued the first report on smoking and health, which concluded that cigarette smoke causes lung cancer. Since then, research on the toxicity and carcinogenicity of tobacco smoke has demonstrated that the health risk from inhaling tobacco smoke is not limited to the smoker, but also includes those who inhale ETS. ETS contains many of the toxic agents and carcinogens that are present in mainstream smoke, but in diluted form. Recent epidemiologic studies support and reinforce earlier published reviews by the Surgeon General and the National Research Council demonstrating that exposure to ETS can cause lung cancer. These reviews estimated the relative risk of lung cancer to be approximately 1.3 for a nonsmoker living with a smoker compared with a nonsmoker living with a nonsmoker. In addition, recent evidence suggests a possible association between exposure of nonsmokers to ETS and an increased risk of heart disease.

Although these data were not gathered in an occupational setting, ETS meets the criteria of the Occupational Safety and Health Administration (OSHA) for classifying substances as potential occupational carcinogens [Title 29 of the Code of Federal Regulations, Part 1990]. NIOSH therefore recommends that ETS be regarded as a potential occupational carcinogen in conformance with the OSHA carcinogen policy, and that exposures to ETS be reduced to the lowest feasible concentration. Employers should minimize occupational exposure to ETS by using all available preventive measures.

Reports of the Surgeon General on the Health Effects of Tobacco Smoke

In 1964, the Surgeon General issued the first report on smoking and health, which concluded that cigarette smoke causes cancer [DHEW 1964]: Cigarette smoking is causally related to lung cancer in men; the magnitude of the effect of cigarette smoking far outweighs all other factors. The data for women, though less extensive, point in the same direction...The risk of developing lung cancer increases with duration of smoking and the number of cigarettes smoked per day, and is diminished by discontinuing smoking.

Since 1964, evidence has continued to support the causal relationship between exposure to cigarette smoke and lung cancer, demonstrating that risk increases with amount and duration of smoking. Subsequent research has increased our knowledge about the toxicity and carcinogenicity of tobacco smoke and the risks of exposure. Additional support for the Surgeon General's conclusion has come from (1) animal studies that demonstrated the carcinogenicity of tobacco smoke condensate, and (2) analytical studies demonstrating that tobacco smoke contains carcinogens [DHEW 1972; DHHS 1982]. Cigarette smoking is the major cause of lung cancer (87% of lung cancer deaths) and is estimated to account for 30% of all cancer deaths [DHHS 1989].

The 1964 Surgeon General's report also pointed out that male cigarette smokers have higher death rates from heart disease than nonsmokers. Subsequent reports have concluded that cigarette smoking is a major cause of heart disease and that smoking is a major independent risk factor for heart attack [DHEW 1968; DHHS 1983]. On July 1, 1965, Congress approved the Federal Cigarette Labeling and Advertising Act of 1965 (Public Law 89-92). This law, which became effective on January 1, 1966, was the first of a continuing series of Federal statutes enacting warning labels to inform the public about the health hazards of smoking and, subsequently, the use of other tobacco products. Presently, the Comprehensive Smoking Education Act (Public Law 98-474) [Title 15, 1331 of the U.S. Code] requires cigarette companies to rotate four health warnings on all cigarette packages and in advertisements.

Comparison of the Chemical Composition of ETS and MS

ETS contains many of the toxic agents and carcinogens that are present in MS, but in diluted form [DHHS 1986]. The major source of ETS is sidestream smoke*** (SS), which contains higher amounts of some toxic and carcinogenic agents than MS when it is obtained in its undiluted form under laboratory conditions [DHHS 1989]. For example, the release of volatile N-nitrosamines and aromatic amines is higher in SS than in MS.

A major reason that undiluted SS and MS have different concentrations of toxic and carcinogenic agents is that peak temperatures in the burning cone of a cigarette reach 800 to 900C during puffing, but only 600C between puffs, resulting in less complete combustion of tobacco during generation of SS. In addition, most of the burning cone is oxygen deficient during smoldering and produces a strongly reducing environment [NRC 1986]. Table 1 lists 26 toxic and carcinogenic agents identified in SS and MS.

ETS is diluted in the air before it is inhaled and thus is less concentrated than MS. However, active inhalation of MS is limited to the time it takes to smoke each cigarette, whereas exposure to ETS is constant over the period spent in the ETS-polluted environment. This fact is reflected in measurements of nicotine uptake by smokers and ETS-exposed nonsmokers [DHHS 1989].

Potential for Occupational Exposure

Approximately 29% of the U.S. adult population smokes cigarettes, and exposure to ETS is common [DHHS 1989]. Many people who report no exposure to ETS have low concentrations of cotinine (a metabolite of nicotine) in their urine, indicating exposure. The average concentration of cotinine in the urine of nonsmokers has been reported to be approximately 8 ng/ml compared with approximately 1,200 ng/ml in smokers [Cummings et al. 1990]. The National Research Council (NRC) estimated that nonsmokers exposed to ETS averaged 25 ng of urinary cotinine/ml, and active smokers averaged 1,825 ng/ml [NRC 1986]. Husgafvel-Pursiainen et al. [1987] found that nonsmoking restaurant workers had an average urinary cotinine concentration of 56 ng/ml, and nonsmokers not exposed to ETS had an average concentration of 8.3 ng/ml. Other investigators have shown that nonsmokers living with smokers have approximately two to three times the amount of urinary cotinine as nonsmokers living with nonsmokers [Haley et al. 1989].

Table 1.
Toxic and carcinogenic agents in undiluted cigarette SS*,**

Compound

Type of toxicity

Amount in SS
(per cigarette)

Ratio of SS/MS

Vapor phase:

Carbon Monoxide

T

26.8-61 mg

2.5-14.9

Carbonyl Sulfide

T

2-3 mg

0.03-0.13

Benzene

C

400-500 g

8-10

Formaldehyde

C

1,500 g

50

3-Vinylpyridine

SC

300-450 g

24-34

Hydrogen Cyanide

T

14-110 g

0.06-0.4

Hydrazine

C

90 ng

3

Nitrogen Oxides (NOx)

T

500-2,000 g

3.7-12.8

N-nitrosodimethylamine

C

200-1,040 ng

20-130

N-nitrosopyrrolidine

C

30-390 ng

6-120

Particulate phase:

Tar

C

14-30 mg

1.1-15.7

Nicotine

T

2.1-46 mg

1.3-21

Phenol

TP

70-250 g

1.3-3.0

Catechol

CoC

58-290 g

0.67-12.8

o-Toluidine

C

3 g

18.7

2-Naphthylamine

C

70 ng

39

4-Aminobiphenyl

C

140 ng

3.1

Benz(a)anthracene

C

40-200 ng

2-4

Benzo(a)pyrene

C

40-70 ng

2.5-20

Quinoline

C

15-20 g

8-11

N-nitrosonomicotine

C

0.15-1.7 g

0.5-5.0

NNK

C

0.2-1.4 g

1.0-22

N-nitrosodiethanolamine

C

43 ng

1.2

Cadmium

C

0.72 g

7.2

Nickel

C

0.2-2.5 g

13-30

Polonium-210

C

0.5-1.6 pCi

1.06-3.7

*Sources: DHHS [1989]; Hoffmann and Hecht [1989]. [return to table]
**Abbreviations: C, carcinogenic; CoC, cocarcinogenic; MS, mainstream smoke; SC, suspected carcinogen; SS, sidestream smoke; T, toxic; TP, tumor promoter, NNK, 4-(methyl-nitrosamino)-(3-pyridyl)-1-butanone. [return to table]

Exposures to ETS were measured by respirable suspended particulates (2.5 m) and averaged 242 g/m3 in public access buildings [First 1984; NRC 1986; Repace and Lowrey 1980, 1982]. Studies reviewed by [Repace and Lowrey 1990] suggested a 62% probability of exposure to ETS for a nonsmoker in the workplace. However, the relative contribution of work versus home environments in ETS exposure has not been well quantified. In addition, social settings outside the workplace or the home (e.g., restaurants and bowling alleys) may contribute significantly to ETS exposure.

On the basis of urinary cotinine concentrations, the [NRC 1986] concluded that nonsmokers exposed to ETS absorb the equivalent of 0.1 to 1.0 cigarette per day. On the basis of 1985 data, NIOSH estimates that each cigarette smoker in the United States smokes an average of about 21 cigarettes per day [NCHS 1988]. Blood and urine samples analyzed for vapor phase nicotine indicate that nonsmokers exposed to ETS absorb about 1% of the tobacco combustion products absorbed by active smokers [NRC 1986; DHHS 1986].

Reference Key:

SS - sidestream smoke (smoke generated by smoldering tobacco between puffs and smoke diffusing through the cigarette paper and escaping from the burning cone during puffing)
MS - mainstream smoke (smoke drawn through the tobacco and into the smoker's mouth)

Table 2.
Recent Studies of Lung Cancer Among ETS-Exposed Persons Who Never Smoked

Study

Design

Exposure Definition

Relative Risk

Comments

Update of Gillis et al. [1984] by Hole et al. [1989]

12-yr followup, 3,960 men and 4,037 women aged 45-64 in1972-76

Living with smoker or ex-smoker at the time of the survey

2.41 (CI, 0.45-12.83; 7 observed)

Adjusted for age, sex, and social class

Brownson et al. [1987]

19 cases, 47 controls

Exposure for >4 hr /day

1.68 (CI, 0.39-2.97)

Adjusted for age, income, and occupation

Humble et al. [1987]

28 cases, 54 controls

Lived with a spouse who smoked

For cigarette ETS exposure: 2.2 (90% CI, 1.0-4.9)

For any type of ETS exposure: 2.6 (90% CI, 1.2-5.6)

Adjusted for ethnicity and age

Gao et al. [1987]

246 cases, 375 controls

Lived with a smoker

<20 yr, 1.0; 20-29 yr, 1.1 (CI, 0.7-1.8); 30-39 yr, 1.3 (CI, 0.8-2.1); >40 yr, 1.7(CI, 1.0-2.9)

Adjusted for age and education

Lam et al. [1987]

199 cases, 335 controls

Lived with a spouse who smoked

1.65 (CI, 1.16-2.35)

Matched for age and neighborhood

Janerich et al. [1990]

191 cases, 191 controls

>25 smoker-yr of exposure during childhood

2.07 (CI, 1.16-3.68)

Matched for age, sex, and county of residence; relative risk for spousal smoking = 0.9

Shimizu et al. [1988]

90 cases, 163 controls

Lived with mother who smoked Lived with father-in-law who smoked

4.0 (P<0.05)
3.2 (P<0.05)

Matched for age, sex, and hospital; relative risk for spousal smoking = 1. 1

Geng et al. [1988]

54 cases, 93 controls

Lived with spouse who smoked

2.16 (CI, 1.03-4.53)

Matched for race, age, sex, and marital status; positive dose response; methodologic details not presented

*Confidence interval is 95 % unless otherwise indicated

Conclusions

In 1964 the Surgeon General concluded that cigarette smoke causes lung cancer. Since that time, additional research on the toxicity and carcinogenicity of tobacco smoke has demonstrated that the health risks from inhaling tobacco smoke are not limited to smokers, but also include those who inhale ETS. ETS contains many of the toxic agents and carcinogens found in MS, but in diluted form. Recent epidemiologic studies support and reinforce the conclusions of the reviews by the Surgeon General and the NRC demonstrating that exposure to ETS can cause lung cancer. These reviews estimated the relative risk for lung cancer to be approximately 1.3 for nonsmokers living with smokers compared with nonsmokers living with nonsmokers. In addition, recent evidence also suggests a possible association between exposure to ETS and an increased risk for heart disease in nonsmokers. The recent epidemiologic studies (including those associating ETS with other adverse health effects) point to a pattern of health effects that is similar for both smokers and nonsmokers exposed to ETS.

NIOSH recognizes that these recent epidemiologic studies have several shortcomings: lack of objective measures for characterizing and quantifying exposures, failure to adjust for all confounding variables, potential misclassification of exsmokers as nonsmokers, unavailability of comparison groups that have not been exposed to ETS, and low statistical power. Nonetheless, NIOSH has determined that the collective weight of evidence (i.e., that from the Surgeon General's reports, the similarities in composition of MS and ETS, and the recent epidemiologic studies) is sufficient to conclude that ETS poses an increased risk of lung cancer and possibly heart disease to occupationally exposed workers. The epidemiologic data are not sufficient to draw conclusions about other health effects such as cervical cancer, ischemic stroke, spontaneous abortion, and low birthweight.

Recommendations

Several systems exist for classifying a substance as a carcinogen. Such classification systems have been developed by NTP [1989], IARC [1987], and OSHA [29 CFR 1990]. NIOSH considers the OSHA classification system (Identification, Classification, and Regulation of Potential Occupational Carcinogens [29 CFR 1990], also known as the OSHA carcinogen policy) the most appropriate for use in identifying occupational carcinogens. The Surgeon General has concluded that cigarette smoke causes lung cancer as well as heart disease. Table 1 lists 21 known or suspected carcinogens, cocarcinogens, and tumor promoters identified as components of ETS and MS in analytical studies. Furthermore, a large body of evidence indicates that exposure to ETS has produced lung cancer in nonsmokers. NIOSH therefore considers ETS to be a potential occupational carcinogen in conformance with the OSHA carcinogen policy [29 CFR 1990].

The risk of developing cancer should be decreased by minimizing exposure to ETS. Employers should therefore assess conditions that may result in worker exposure to ETS and take steps to reduce exposures to the lowest feasible concentration.

Methods for Controlling Involuntary Exposure to ETS

Workers should not be involuntarily exposed to tobacco smoke. To prevent worker exposures to any hazardous substance, employers should first eliminate hazardous workplace emissions at their source. If elimination is not possible, emissions should be removed from the pathway between the source and the worker [NIOSH 1983]. Therefore, the best method for controlling worker exposure to ETS is to eliminate tobacco use from the workplace and to implement a smoking cessation program. Until tobacco use can be completely eliminated, employers should protect nonsmokers from ETS by isolating smokers. Methods for eliminating tobacco use from the workplace and isolating smokers are described here briefly.

Eliminating Tobacco Use from the Workplace

Worker exposure to ETS is most efficiently and completely controlled by simply eliminating tobacco use from the workplace. To facilitate elimination of tobacco use, employers should implement smoking cessation programs. The Association of Schools of Public Health (ASPH) has recommended the following strategy for smoking cessation [NIOSH 1986]. Specifically, management and labor should work together to develop appropriate nonsmoking policies that include some or all of the following:

Worker exposure to ETS is most efficiently and completely controlled by simply eliminating tobacco use from the workplace. To facilitate elimination of tobacco use, employers should implement smoking cessation programs. The Association of Schools of Public Health (ASPH) has recommended the following strategy for smoking cessation [NIOSH 1986]. Specifically, management and labor should work together to develop appropriate nonsmoking policies that include some or all of the following:

1.)  

Prohibit smoking at the workplace and provide sufficient disincentives for those who do not comply

2.)  

Distribute information about health promotion and the harmful effects of smoking

3.)  

Offer smoking-cessation classes to all workers

4.)  

Establish incentives to encourage workers to stop smoking

5.)  

Further information regarding workplace smoking policies and smoking cessation programs can be found in No Smoking: A Decision Maker's Guide to Reducing Smoking at the Worksite [American Cancer Society et al. 1985].

Isolating Smokers

The 1986 Surgeon General's report on involuntary smoking concluded that, the simple separation of smokers and nonsmokers within the same airspace may reduce, but does not eliminate, the exposure of nonsmokers to ETS. In indoor workplaces where smoking is permitted, ETS can spread throughout the airspace of all workers. The most direct and effective method of eliminating ETS from the workplace is to prohibit smoking in the workplace. Until that is achieved, employers can designate separate, enclosed areas for smoking, with separate ventilation. Air from this area should be exhausted directly outside and not recirculated within the building or mixed with the general dilution ventilation for the building. Ventilation of the smoking area should meet general ventilation standards, and the smoking area should have slight negative pressure to ensure airflow into the area rather than back into the airspace of the workplace [ASHRAE 1989]. Guidance for designing local exhaust ventilation systems can be found in Recommended Industrial Ventilation Guidelines [Hagopian and Bastress 1976], Industrial Ventilation A Manual of Recommended Practice [ACGIH 1986], and Fundamentals Governing the Design and Operation of Local Exhaust Systems [ANSI 1979].

Warning signs should be posted at the entrances to the workplace in both English and the predominant language of non-English-reading workers. These signs should state that smoking is prohibited or permitted only in designated smoking areas. If designated smoking areas are provided, they should be clearly identified by signs.

POSITIONS OF OTHER AGENCIES REGARDING ETS

The Occupational Safety and Health Administration (OSHA) and the Mine Safety and Health Administration (MSHA) have not established permissible exposure limits (PELs) for ETS in the workplace. OSHA is now preparing to address this issue as part of an indoor air quality standard.

The U.S. Environmental Protection Agency (EPA) states that ETS is a known cause of lung cancer and respiratory symptoms and that it has been linked to heart disease. EPA also recommends that exposure to ETS be minimized wherever possible by restricting smoking to separately ventilated areas directly exhausted to the outside, or by entirely eliminating smoking in buildings [EPA 1989].

The International Agency for Research on Cancer [IARC 1986] states that epidemiologic studies have demonstrated an increased risk of lung cancer for nonsmoking spouses of smokers. Although researchers had substantial difficulty in determining exposure to ETS and other risk factors for the cancers studied, IARC concluded that passive smoking gives rise to some risk of cancer. IARC also concluded that there is sufficient evidence that tobacco smoke is carcinogenic to humans, and that there is sufficient evidence that inhalation of tobacco smoke as well as topical application of tobacco smoke condensate cause cancer in experimental animals.

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