Work, a segregated social context in the United States, may be an important source of differential exposure to stress by race/ethnicity, but existing research does not systematically describe variation in exposure to occupational stress by race/ethnicity. Using work history data from the U.S. Health and Retirement Study and occupational-level measures from the Bureau of Labor Statistics and the Occupational Information Network, the authors document the extent to which the race/ethnicity and gender composition of occupational categories varies by level of occupational strain and how life-course exposure to occupational strain differs by race/ethnicity and gender. Black and Latino workers are overrepresented in high-strain jobs at many ages, compared with other groups. Exposure to job strain across working ages shows more variation in exposure by gender and race/ethnicity groups than static measures. These findings point to potential bias in research using a single, cross-sectional measure of job stress.

Latinos in the US live significantly longer than non-Latino whites, but spend more years disabled. Differentials in socioeconomic status account for part, but not all, of the difference in older age disability between Latinos and whites. We hypothesize that a factor often ignored in the literature-the fact that Latinos, on average, have more physically strenuous jobs than non-Latino whites-contributes to the higher Latino risk of functional limitations at older ages. We use longitudinal data from the 1998-2014 Health and Retirement Study (HRS) comprising 17,297 respondents. Compared to US-born whites, Latinos, especially Latino immigrants, report substantially higher levels of physical effort at work. Latino-black differences are much smaller than Latino-white differences. As hypothesized, physical work effort is strongly related to functional limitations. However, differentials in physical work effort for Latinos and whites in their fifties and early sixties are weakly related to Latino-white differentials in FL at later ages.

Few studies have examined the relationship between ambient polycyclic aromatic hydrocarbons (PAHs) and pulmonary function in children. Major sources include vehicular emissions, home heating, wildland fires, agricultural burning, and power plants. PAHs are an important component of fine particulate matter that has been linked to respiratory health. This cross-sectional study examines the relationship between estimated individual exposures to the sum of PAHs with 4, 5, or 6 rings (PAH456) and pulmonary function tests (forced expiratory volume in one second (FEV1) and forced expiratory flow between 25% and 75% of vital capacity) in asthmatic and non-asthmatic children. We applied land-use regression to estimate individual exposures to ambient PAHs for averaging periods ranging from 1 week to 1 year. We used linear regression to estimate the relationship between exposure to PAH456 with pre- and postbronchodilator pulmonary function tests in children in Fresno, California (N=297). Among non-asthmatics, there was a statistically significant association between PAH456 during the previous 3 months, 6 months, and 1 year and postbronchodilator FEV1. The magnitude of the association increased with the length of the averaging period ranging from 60 to 110 ml decrease in FEV1 for each 1 ng/m(3) increase in PAH456. There were no associations with PAH456 observed among asthmatic children. We identified an association between annual PAHs and chronic pulmonary function in children without asthma. Additional studies are needed to further explore the association between exposure to PAHs and pulmonary function, especially with regard to differential effects between asthmatic and non-asthmatic children.

BACKGROUND: Although studies have demonstrated that air pollution is associated with exacerbation of asthma symptoms in children with asthma, little is known about the susceptibility of subgroups, particularly those with atopy. OBJECTIVE: This study was designed to evaluate our a priori hypothesis that identifiable subgroups of asthmatic children are more likely to wheeze with exposure to ambient air pollution. METHODS: A cohort of 315 children with asthma, 6-11 years of age, was recruited for longitudinal follow-up in Fresno, California (USA). During the baseline visit, children were administered a respiratory symptom questionnaire and allergen skin-prick test. Three times a year, participants completed 14-day panels during which they answered symptom questions twice daily. Ambient air quality data from a central monitoring station were used to assign exposures to the following pollutants: particulate matter <= 2.5 mu m in aerodynamic diameter, particulate matter between 2.5 and 10 mu m in aerodynamic diameter (PM(10-2.5)), elemental carbon, nitrogen dioxide (NO(2)), nitrate, and O(3). RESULTS: For the group as a whole, wheeze was significantly associated with short-term exposures to NO(2) [odds ratio (OR) = 1.10 for 8.7-ppb increase; 95% confidence interval (CI), 1.02-1.20] and PM(10-2.5) (OR = 1.11 for 14.7-mu g/m(3) increase; 95% CI, 1.01-1.22). The association with wheeze was stronger for these two pollutants in children who were skin-test positive to cat or common fungi and in boys with mild intermittent asthma. CONCLUSION: A pollutant associated with traffic emissions, NO(2), and a pollutant with bioactive constituents, PM(10-2.5), were associated with increased risk of wheeze in asthmatic children living in Fresno, California. Children with atopy to cat or common fungi and boys with mild intermittent asthma were the subgroups for which we observed the largest associations.