Emerging research suggests environmental exposures before conception may adversely affect allergies and lung diseases in future generations. Most studies are limited as they have focused on single exposures, not considering that these diseases have a multifactorial origin in which environmental and lifestyle factors are likely to interact. Traditional exposure assessment methods fail to capture the interactions among environmental exposures and their impact on fundamental biological processes, as well as individual and temporal factors. A valid estimation of exposure preconception is difficult since the human reproductive cycle spans decades and the access to germ cells is limited. The exposome is defined as the cumulative measure of external exposures on an organism (external exposome), and the associated biological responses (endogenous exposome) throughout the lifespan, from conception and onwards. An exposome approach implies a targeted or agnostic analysis of the concurrent and temporal multiple exposures, and may, together with recent technological advances, improve the assessment of the environmental contributors to health and disease. This review describes the current knowledge on preconception environmental exposures as related to respiratory health outcomes in offspring. We discuss the usefulness and feasibility of using an exposome approach in this research, advocating for the preconception exposure window to become included in the exposome concept.

Altered gene expression in pathways relevant to leukaemogenesis, as well as reduced levels of circulating lymphocytes, have been reported in workers that were exposed to benzene concentrations below 1 ppm. In this study, we analysed whole blood global gene expression patterns in a worker cohort with altered levels of T cells and immunoglobulins IgM and IgA at three time points; pre-shift, post-shift (after three days), and post-recovery (12 hours later). Eight benzene exposed tank workers performing maintenance work in crude oil cargo tanks with a mean benzene exposure of 0.3 ppm (range 0.1–0.5 ppm) and five referents considered to be unexposed were examined by gene expression arrays. By using our data as independent validation, we reanalysed selected genes that were reported to be altered from previous studies of workers being exposed to sub-ppm benzene levels Four out of six genes previously proposed as marker genes in chronically exposed workers separated benzene exposed workers from unexposed referents (CLEC5, ACSL1, PRG2, IFNB1). Even better separation of benzene exposed workers and referents was observed for short-term exposure for genes in the Jak-STAT pathway, particularly elevated expression of IL6 and reduced expression of IL19.

In a recent study we found that fathers’ but not mothers’ onset of overweight in puberty was associated with asthma in adult offspring. The potential impact on offspring’s adult lung function, a key marker of general and respiratory health, has not been studied. We investigated the potential causal effects of parents’ overweight on adult offspring’s lung function within the paternal and maternal lines. We included 929 offspring (aged 18–54, 54% daughters) of 308 fathers and 388 mothers (aged 40–66). Counterfactual-based multi-group mediation analyses by offspring’s sex (potential moderator) were used, with offspring’s prepubertal overweight and/or adult height as potential mediators. Unknown confounding was addressed by simulation analyses. Fathers’ overweight before puberty had a negative indirect effect, mediated through sons’ height, on sons’ forced expiratory volume in one second (FEV₁) (beta (95% CI): −144 (−272, −23) mL) and forced vital capacity (FVC) (beta (95% CI): −210 (−380, −34) mL), and a negative direct effect on sons’ FVC (beta (95% CI): −262 (−501, −9) mL); statistically significant effects on FEV₁/FVC were not observed. Mothers’ overweight before puberty had neither direct nor indirect effects on offspring’s lung function. Fathers’ overweight starting before puberty appears to cause lower FEV₁ and FVC in their future sons. The effects were partly mediated through sons’ adult height but not through sons’ prepubertal overweight.