Air Pollution, Smoking, and Plasma Homocysteine

Abstract

Mild hyperhomocysteinemia is independently associated with an increased risk of cardiovascular disease. Air pollution exposure induces short-term inflammatory changes that may determine hyperhomocysteinemia, particularly in the presence of a preexisting proinflammatory status such as that found in cigarette smokers. We examined the relation of air pollution levels with fasting and postmethionine-load total homocysteine (tHcy) in 1,213 normal subjects from Lombardia, Italy. We obtained hourly concentrations of particulate matter < 10 mum in aerodynamic diameter (PM(10)) and gaseous pollutants (carbon monoxide, nitrogen dioxide, sulfur dioxide(,) ozone) from 53 monitoring sites covering the study area. We applied generalized additive models to compute standardized regression coefficients controlled for age, sex, body mass index, smoking, alcohol, hormone use, temperature, day of the year, and long-term trends. The estimated difference in tHcy associated with an interquartile increase in average PM(10) concentrations in the 24 hr before the study was nonsignificant [0.4%; 95% confidence interval (CI), -2.4 to 3.3 for fasting; and 1.1%, 95% CI, -1.5 to 3.7 for postmethionine-load tHcy]. In smokers, 24-hr PM(10) levels were associated with 6.3% (95% CI, 1.3 to 11.6; p < 0.05) and 4.9% (95% CI, 0.5 to 9.6; p < 0.05) increases in fasting and postmethionine-load tHcy, respectively, but no association was seen in nonsmokers (p-interaction = 0.005 for fasting and 0.039 for postmethionine-load tHcy). Average 24-hr O(3) concentrations were associated with significant differences in fasting tHcy (6.7%; 95% CI, 0.9 to 12.8; p < 0.05), but no consistent associations were found when postmethionine-load tHcy and/or 7-day average O(3) concentrations were considered. Air particles may interact with cigarette smoking and increase plasma homocysteine in healthy subjects.