Abstract
Limited data are available on seasonal associations of polycyclic aromatic hydrocarbons (PAHs) exposure with oxidative DNA damage. We conducted a pilot study with 20 postgraduates, and measured urinary levels of mono-hydroxyl PAHs (OH-PAHs) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) for 7 consecutive days in the four seasons. We assessed the relationships of urinary OH-PAHs with urinary 8-OHdG in the whole year as well as cold- and warm-seasons. Summed OH-PAHs (∑OH-PAHs) were higher in cold season than in warm season. Each ln-unit (ln-transformed unit) increase in ∑OH-PAHs in the whole year corresponded to a 34%, 16% or 23% increase in urinary 8-OHdG levels at lag0, lag1 or lag2 day as well as a 26% increase in urinary 8-OHdG levels at lag0-2 days (cumulative effects). Each ln-unit increase in ∑OH-PAHs corresponded to a 36%, 26% or 46% increase in urinary 8-OHdG levels in cold season at lag0 day, lag1 day or lag2 day as well as a 36% increase in urinary 8-OHdG in warm season at lag0 day. Distributed non-linear cumulative lag models (DLNMs) indicated that each ln-unit increase in ∑OH-PAHs within the range of 5.7–8.1 nmol/mmol Cr had a stronger effect (coefficient β: 1.11–2.97 nmol/mmol Cr) on urinary 8-OHdG rather than non-cumulative DLNMs (coefficient β: 1.08–1.43 nmol/mmol Cr) as well as the non-linear dose-response relationships of ∑OH-PAHs with urinary 8-OHdG. PAHs exposure exhibited the lagged and cumulative effects on urinary 8-OHdG levels.
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