RESUMO
Aflatoxins are a group of naturally occurring mycotoxins, which can lead to death and are a known cause of hepatocellular carcinoma. AF exposure has been hypothesised to lead to stunted growth in children, but separating the AF effect from other determinants of linear growth retardation is difficult. The study used secondary data from an efficacy trial conducted in young children in southern Mexico to test the comparative efficacy of a milk-based multiple micronutrient-fortified food, a multiple micronutrient syrup, or a multiple micronutrient powder. The effect of serum AFB1 -lysine adduct level on incremental growth was tested using a longitudinal mixed model, controlling for key individual, maternal, and household-level covariates. AFB1 -lysine adduct was detectable in all but 2 of the 347 children in the study (median exposure: 0.82 pg/mg albumin). AF exposure was associated (p < .05) with greater linear growth: an increase equivalent to the sample interquartile range (~0.5 pg AFB1 -lysine/mg albumin) was associated (p < .05) with an increase in the child's height-for-age deficit of 1.5 to 2.0 mm in the 4 months from baseline (average age 8 months) to follow-up (average age 12 months); the magnitude of the difference in the 10-month follow-up was smaller and not statistically significant. This study documents that low-dose AF exposure was associated with greater child linear growth. Given its toxicity and carcinogenicity, our results do not change the urgent need to drastically reduce human AF exposure. Our findings show that the association between AF exposure and linear growth is more complex than previously thought.
Assuntos
Aflatoxina B1/sangue , Estatura/fisiologia , Exposição Ambiental/estatística & dados numéricos , Lisina/sangue , Dieta/estatística & dados numéricos , Exposição Ambiental/análise , Feminino , Contaminação de Alimentos , Humanos , Lactente , Estudos Longitudinais , Masculino , México/epidemiologiaRESUMO
Nearly half of the world's population is exposed to household air pollution (HAP) due to long hours spent in close proximity to unvented cooking fires. The effect of woodsmoke exposure on oxidative stress was examined by investigating the association between woodsmoke exposure and biomarkers of DNA oxidation (8-hydroxy-2'-deoxyguanosine [8-OHdG]) and lipid peroxidation (8-isoprostane) among control and intervention stove users. HAP exposure assessment was conducted within the framework of a community-randomized controlled trial of 51 communities in San Marcos Province, Cajamarca Region, Peru. The first morning urine voids after 48h HAP exposure assessment from a subset of 45 control and 39 intervention stove users were analyzed for 8-OHdG and 8-isoprostane. General linear models and correlation analyses were performed. Urinary oxidative stress biomarkers ranged from 11.2 to 2270.0µg/g creatinine (median: 132.6µg/g creatinine) for 8-OHdG and from 0.1 to 4.5µg/g creatinine (median: 0.8µg/g creatinine) for 8-isoprostane among all study subjects (n=84). After controlling for the effects of traffic in the community and eating food exposed to fire among all subjects, cooking time was weakly, but positively associated with urinary 8-OHdG (r=0.29, p=0.01, n=80). Subjects' real-time personal CO exposures were negatively associated with 8-OHdG, particularly the maximum 30-second CO exposure during the sampling period (r=-0.32, p=0.001, n=73). 48h time integrated personal PM2.5 was negatively, but marginally associated with urinary 8-isoprostane (r=-0.21, p=0.09, n=69) after controlling for the effect of distance of homes to the road. Urinary 8-isoprostane levels reported in the available literature are comparable to results found in the current study. However there were relatively high levels of urinary 8-OHdG compared to data in the available literature for 8-OHdG excretion. Results suggest a sustained systemic oxidative stress among these Peruvian women chronically exposed to wood smoke.