Journal of Occupational & Environmental Medicine:
Declining Trends in Serum Cotinine Levels in US Worker Groups: the Power of Policy
Arheart, Kristopher L. EdD; Lee, David J. PhD; Dietz, Noella A. PhD; Wilkinson, James D. MD, MPH; Clark, John D. III MS; LeBlanc, William G. PhD; Serdar, Berrin MD, PhD; Fleming, Lora E. MD, PhD
From the Department of Epidemiology and Public Health (Drs Arheart, Lee, Dietz, Wilkinson, LeBlanc, and Fleming and Mr Clark); Sylvester Comprehensive Cancer Center (Drs Lee, Dietz, Wilkinson, and Fleming), University of Miami Miller School of Medicine; and School of Public Health (Dr Serdar), Florida International University, Miami, Fla.
Address correspondence to: Lora E. Fleming, MD, PhD, Department of Epidemiology and Public Health, University of Miami School of Medicine, P.O. Box 016069 (R-669), Miami, FL 33101; E-mail: email@example.com.
Objective: To explore trends in cotinine levels in US worker groups.
Methods: Using NHANES III data, serum cotinine levels of US workers not smokers nor exposed to secondhand smoke (SHS) at home were evaluated for trends by occupational/industrial and race/ethnicity-gender sub-groups.
Results: Decreases from 1988 to 2002 ranged from 0.08 to 0.30 ng/mL (67% to 85% relative decrease), with largest absolute reductions in: blue-collar and service occupations; construction/manufacturing industrial sectors; non-Hispanic Black male workers.
Conclusions: All worker groups had declining serum cotinine levels. Most dramatic reductions occurred in sub-groups with the highest before cotinine levels, thus disparities in SHS workforce exposure are diminishing with increased adoption of clean indoor laws. However, Black male workers, construction/manufacturing sector workers, and blue-collar and service workers have the highest cotinine levels. Further reductions in SHS exposure will require widespread adoption of workplace clean air laws without exemptions.
The US Surgeon General has recently concluded that secondhand smoke (SHS) causes premature death and disease in adults who do not smoke, and that there is no scientific evidence of a risk-free level of exposure.1 The combined indirect and direct economic costs of SHS exposure total approximately 10 billion dollars annually.2 This is likely an underestimate because it does not include costs associated with health outcomes not yet determined to be causally associated with SHS (eg, breast cancer).3 Recent meta-analysis of occupational studies suggest a 24% increased risk of lung cancer in workers exposed to SHS smoke on the job, with an even greater risk noted in highly exposed workers (relative risk 2.1; 95% confidence interval: 1.3 to 2.6).4
As documented by the National Health and Nutrition Examination Survey (NHANES), there have been dramatic reductions in the serum cotinine levels in the US population.5 These reductions can be attributed, in part, to the successful passage of clean indoor air legislation at the state and local levels. For example, there is evidence that residing in communities with strong clean indoor air legislation is highly associated with reduced SHS exposures as verified by serum cotinine levels.6
Although rates are dropping in the United States, the worksite remains a significant source of SHS exposure for millions of US workers.7,8 Occupational exposure can be considerable, with levels up to four times that of household exposures.9 Numerous studies also have documented that occupational SHS exposures are not equally distributed across different worker groups. For example, food service workers, especially bartenders and waitstaff, report the lowest rates of smoke-free workplace policies at their places of employment.10
Blue-collar workers and select service workers typically have higher rates of SHS occupational exposure relative to White-collar workers.11 These higher rates are of particular concern because many blue-collar workers have occupational chemical and dust exposures which may adversely and synergistically impact upon SHS-associated health outcomes (eg, dust and fumes and increased risk of asthma and allergic sensitization).12,13 Several studies have noted stronger lung cancer associations for occupational versus household SHS exposures, particularly among female workers.14,15
This study explored changes in serum cotinine levels in representative samples of non-smoking US workers with no reported tobacco smoke exposure at home.
The National Center for Health Statistics (NCHS) conducted the NHANES III study in two phases: from 1988 to 1991 and from 1991 to 1994. A complex sampling strategy was used to obtain a representative sample of Blacks, non-Hispanic Whites, and Mexican-Americans, aged 2 months and older.16 Household interviews were obtained on nearly 34,000 family members from approximately 20,000 randomly selected households in 81 counties. Physical examinations were conducted at mobile examination centers where blood samples were obtained. The 1999 to 2000 and 2001 to 2002 NHANES also employed a complex sampling strategy to obtain a representative sample of the US civilian, non-institutionalized population, aged 2 months and older.17 Blacks and Mexican-Americans were over-sampled. Response rates to the physical examination ranged from 76.3% to 79.7%.18–20
The NHANES asked detailed questions about current and longest held job. Using current held job, this permitted a classification based on 1990 US Census Codes,21 using a four-category occupational variable commonly employed by the NCHS which included the categories of White-collar (Census codes 003-389), service workers (403–469), farming, fishing, and forestry (473–499), and blue-collar workers (503–889).22 We also grouped workers into eight industrial sector classifications which are now the focus of the National Occupational Research Agenda at the National Institute on Occupational Safety and Health (NIOSH): Agriculture, forestry, fishing; Mining; Construction; Manufacturing; Wholesale, and retail trade; Transportation, warehousing, utilities; Services; and Health care and social assistance.23 Of note, these industrial groupings ignore the type of work which is done in each sector such that each group may include workers engaged in both blue- and White-collar occupational activities.
In NHANES III and the 1999 to 2000 surveys, serum cotinine was assessed using an isotope dilution, high performance liquid chromatography/atmospheric pressure chemical ionization tandem mass spectrometric method designed to detect levels as low as 0.050 ng/mL.24,25 For the 2001 to 2002 NHANES survey, a similar but more sensitive cotinine assay was used, lowering the detectable limit to 0.015 ng/mL.26 For analysis purposes, the value for data below the detectable limits was the limit divided by the square root of two.27 The difference in lower detection limits did not substantially change the significance of the results.
There were 13,867 workers 18 years of age and older across the four survey periods with available cotinine levels. Our final analytic sample size was 8105 after we applied the following exclusionary criteria: 1) self-reported smoker, 2) presumed smokers with cotinine values greater than 10 ng/mL,23 3) did not have a valid occupational code, and 4) workers who responded “yes” to the question, “Does anyone smoke cigarettes in the home?”
Serum cotinine levels were transformed to natural logarithm values for analysis and are reported as geometric means and 95% confidence bounds. The change from 1988 to 2002 was given as the actual change in ng/mL and as a relative change (percent change). The data were aggregated by subgroups defined by NIOSH industrial sectors, NCHS occupational groups, and race/ethnicity-gender and year, using SAS28 survey procedures to apply the proper weight and adjustment for design effects. Year was defined as the midpoint of the survey period in which the data were collected. In addition to actual sample sizes, we have chosen to present population estimates (Table 1); these must be considered as estimates only because the NHANES sampling scheme was not based on occupational category, but rather on race-ethnicity.
A weighted general linear model was used to calculate statistics for aggregated transformed cotinine means described above. Separate models were run for overall, NIOSH, NCHS, and race/ethnicity-sex groupings. The model included the aggregated transformed cotinine means regressed on subgroups within the major group and year. The inverse of the variance of the cotinine mean was used to weight the regression. The model included separate slopes for each subgroup. Contrasts were used to make pair-wise comparisons between the slopes of the subgroups. The P < 0.05 level was used to determine statistical significance. Of note, the statistical tests in each subset (ie, race-ethnicity) are independent; however, the tests are not independent between subsets. The University of Miami Human subjects Committee approved this study.
The study population of 8164 represented an estimated 70.6 million non-smoking US workers without reported SHS exposure in the home over the four survey periods. Group statistics are given in Table 1. For each group, we reported the number of observations and representative population averaged over the four time periods. The geometric mean and 95% confidence bounds are given for each time period, followed by the actual and relative change from the first to the last time period. The regression statistics are the last items in the table. The regression coefficient and standard error are for log-transformed cotinine values. For the entire sample, there was a significant decrease in cotinine levels (0.16 ng/mL; 80% relative decrease) over time. For each sub-group analysis, there was a steady decline in the mean cotinine levels ranging from 0.08 to 0.31 ng/mL (61% to 85% relative decrease), and a significant negative regression coefficient. All reductions were significant (except for farm workers which had a small subgroup sample size (n = 81)).
In the race/ethnicity-gender groups, the decline in cotinine levels ranged from 0.08 to 0.30 ng/mL (67% to 80% relative decrease) (Fig. 1). The negative slope in cotinine levels for White males was significantly greater (ie, steeper) than the levels for White females and significantly less than for Black males. Black males had significantly greater negative slope than Black females and Mexican-American males. The negative slope in cotinine levels for Black females was significantly greater than the slopes for White females and Mexican-American females.
The decline in cotinine levels for the NCHS occupational categories ranged from 0.10 to 0.22 ng/mL (71% to 76% relative decrease) (Fig. 2). The negative slope in cotinine levels for blue-collar workers and service workers were significantly greater than the slope for White-collar workers.
For the NIOSH industrial sector groups, the decrease in cotinine levels ranged from 0.09 to 0.23 ng/mL (73% to 85% relative decrease) (Fig. 3). The negative slope in cotinine levels for the Construction sector was significantly greater than the slope for Agriculture, health care, and Service sectors. The Manufacturing sector had a larger negative slope than Health care and Service sectors.
Black male workers had the largest absolute reductions in serum cotinine levels of all sub-groups examined, falling 0.30 ng/mL, a 71% relative decrease, over the survey period. Nicotine and cotinine clearance in Black smokers is reportedly lower than in Whites, leading to a longer cotinine half-life in Blacks.29 It is therefore theoretically possible that under identical exposure conditions, Black workers exposed to SHS would exhibit higher cotinine levels relative to White workers. Following this line of argument, Black workers employed in workplaces that implement workplace smoking restrictions would be expected to respond with more dramatic reductions in cotinine levels relative to their White coworkers. Studies in Black male smokers also have demonstrated lower clearance of selected tobacco carcinogens relative to White smokers,30 raising the possibility that reductions in SHS exposure in Black workers may ultimately be more beneficial than in White workers in lowering cancer risk. There is surprisingly little research comparing the health effects of SHS exposed workers as a function of race and ethnicity. Additional research is needed to examine these potential racial differences.
There were several other noteworthy findings including the dramatic reduction in cotinine levels in non-smoking workers from 1998 to 2002. More importantly, many of the large sub-group differences noted in the beginning of the period had diminished over the examined time period. The most dramatic reductions in cotinine levels were evident for workers employed in the construction (0.23 ng/mL; 77% decrease) and manufacturing (0.22 ng/mL; 85% decrease) sectors. When classified by occupation, service and blue-collar workers experienced the most dramatic reductions (0.21 and 0.22 ng/mL, respectively; 76% and 72% decreases).
Although rates are declining, construction workers in particular, and blue-collar workers in general, have the highest smoking rates in the US worker population.31,32 It is possible that SHS exposure levels have dropped most dramatically in these groups, in part, because chronic heavy exposure to tobacco smoke on the job was the norm in many worksites before the implementation of worksite smoking bans. The findings of the present study along with the results of another NHANES-based study showing lower cotinine levels in communities with more comprehensive clean indoor air laws,33 raise the possibility that blue-collar (and service workers) may have particularly benefited from the passage of these laws. Nevertheless, relative to White-collar workers, blue-collar workers have been shown to be least likely to report having a worksite smoking ban at their place of employment.34
Further elimination of the gap in cotinine levels still evident in the present findings will require additional efforts toward universal implementation of worksite smoking restrictions. Furthermore, aggressive implementation of worksite smoking bans leads to lower rates of smoking and reduced smoking levels, as well as changes in social norms, all of which lowers the acceptability of smoking.34,35 Therefore, implementation of smoking restrictions in blue-collar worksites will not only lower SHS exposure in all workers, but could also help address the high rate of smoking in blue-collar worker groups. Partnerships between the tobacco control community and trade unions, which currently represent over 6 million blue-collar and service workers in the United States,36 is one mechanism which can also be used to promote the dissemination of workplace smoking prohibitions.37 The tobacco control community also needs to continue to advocate for comprehensive clean indoor air legislation including comprehensive protection of all workers. Presently, just over half of the US population (52.9%) is protected by laws restricting smoking in at least some workplaces (eg, offices, but not bars).38 However, only 21.7% of the US population resides in states or municipalities with comprehensive clean indoor air legislation which prohibits smoking in all workplaces, including in restaurants and in bars.
Study limitations include the incomplete characterization of SHS exposures outside of the workplace, as well as the availability of only a single cotinine assessment. Serum cotinine has a half-life of 16 to 18 hours so it cannot be considered a measure of chronic exposure to SHS.29 There was likely some measurement error in our analysis because an unknown proportion of the NHANES participants had not worked the day before they provided blood samples for cotinine analysis, therefore reported levels may underestimate the amount of occupational exposure to SHS. On the other hand, the NHANES did not include questions about other forms of SHS exposure such as visiting bars and restaurants, where smoking may still be still permitted; this might lead to an over-estimate of occupational SHS exposure. Although we have excluded likely smokers and those with household SHS exposures from the analysis, we were unable to further exclude those with SHS exposures which occurred in other settings (as well as other sources of nicotine leading to cotinine in the urine, such as food).39,40 Finally, this is an ecological study, and as such a direct causal link between individual smoking cessation and workplace smoking policies can only be inferred, not determined.
To summarize, all examined US worker groups have experienced significant reductions in SHS exposure as measured by serum cotinine levels over the years 1988 to 2002. Disparities in SHS exposure have diminished over the same time period, but large differences in cotinine levels in worker subgroups persist. Black workers, those employed in the construction sector, and blue-collar workers continue to have the highest cotinine levels; additional research is needed to identify factors responsible for this continuing disparity. Further reductions in SHS exposure will be facilitated by widespread adoption of local and state clean air laws that do not exempt any worker groups. Also collaborations between the tobacco control community, unions, and employers need to be pursued concurrently with these policy efforts to increase access to workplace smoking cessation services in addition to rigorous enforcement of workplace smoking prohibitions.
This study was supported by grants from the Flight Attendant Medical Research Institute and the National Institute for Occupational Safety and Health (R01 OH03915).
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