To evaluate exposure estimation methods such as spatially resolved land-use regression models and ambient monitoring data in the context of epidemiological studies of the impact of air pollution on pregnancy outcomes.
The study measured personal 48 h exposures (NO, NO(2), PM(2.5) mass and absorbance) and mobility (time activity and GPS) for 62 pregnant women during 2005-2006 in Vancouver, Canada, one to three times during pregnancy. Measurements were compared to modelled (using land-use regression and interpolation of ambient monitors) outdoor concentrations at subjects' home and work locations.
Personal NO and absorbance (ABS) measurements were moderately correlated (NO: r = 0.54, ABS: r = 0.29) with monitor interpolations and explained primarily within-subject (temporal) variability. Land-use regression estimates including work location improved correlations for NO over those based on home postal code (for NO: r = 0.49 changed to NO: r = 0.55) and explained more between-subject variance (4-20%); limiting to a subset of samples (n = 61) when subjects spent >65% time at home also improved correlations (NO: r = 0.72). Limitations of the GPS equipment precluded assessment of including complete GPS-based mobility information.
The study found moderate agreement between short-term personal measurements and estimates of ambient air pollution at home based on interpolation of ambient monitors and land-use regression. These results support the use of land-use regression models in epidemiological studies, as the ability of such models to characterise high resolution spatial variability is "reflected" in personal exposure measurements, especially when mobility is characterised.
To evaluate the effects of parental occupational chemical exposures on incidence of neuroblastoma in offspring, the authors conducted a multicenter case-control study, using detailed exposure information that allowed examination of specific chemicals. Cases were 538 children aged 19 years who were newly diagnosed with confirmed neuroblastoma in 1992-1994 and were registered at any of 139 participating hospitals in the United States and Canada. One age-matched control for each of 504 cases was selected through random digit dialing. Self-reported exposures were reviewed by an industrial hygienist, and improbable exposures were reclassified. Effect estimates were calculated using unconditional logistic regression, adjusting for child's age and maternal demographic factors. Maternal exposures to most chemicals were not associated with neuroblastoma. Paternal exposures to hydrocarbons such as diesel fuel (odds ratio (OR) = 1.5; 95% confidence interval (CI): 0.8, 2.6), lacquer thinner (OR = 3.5; 95% CI: 1.6, 7.8), and turpentine (OR = 10.4; 95% CI: 2.4, 44.8) were associated with an increased incidence of neuroblastoma, as were exposures to wood dust (OR = 1.5; 95% CI: 0.8, 2.8) and solders (OR = 2.6; 95% CI: 0.9, 7.1). The detailed exposure information available in this study has provided additional clues about the role of parental occupation as a risk factor for neuroblastoma.
Wood dust has been classified as a human carcinogen by the International Agency for Research on Cancer with a footnote that the evaluation was based on a marked excess of sino-nasal cancer among workers exposed primarily to hardwood dusts. Because the epidemiologic data on the carcinogenic effects of softwoods are weaker than for hardwoods, standard setting for softwood dust presents a greater dilemma. Unfortunately, the studies of wood dust and cancer do not have the quantitative exposure data necessary for standard setting for either hardwoods or softwoods. Asthma, non-asthmatic airflow obstruction, and both upper and lower respiratory symptoms have been associated with exposure to both 'allergenic' and 'non-allergenic' softwood dusts, and an association with increasing intensity of exposure has been observed in multiple studies. The available evidence seems to indicate that to prevent these nonmalignant effects, the level of exposure to all softwood dust should be at least as low 2 mg/m3. A standard of 1 mg/m3 may be more appropriate to provide a safety margin to protect more sensitive workers. It may be that some of the health effects observed are due to the natural components of wood, such as resin acids or monoterpenes, or to molds.