Low level aflatoxin exposure associated with greater linear growth in southern Mexico: A longitudinal study

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Abstract

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 AFB 1 ‐lysine adduct level on incremental growth was tested using a longitudinal mixed model, controlling for key individual, maternal, and household‐level covariates. AFB 1 ‐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 AFB 1 ‐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.

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Aflatoxins and growth impairment: a review.

Pornsri Khlangwiset, Felicia Wu, G S Shephard (2011)

Aflatoxins, fungal toxins produced by Aspergillus flavus and Aspergillus parasiticus in a variety of food crops, are well known as potent human hepatocarcinogens. Relatively less highlighted in the literature is the association between aflatoxin and growth impairment in children. Foodborne aflatoxin exposure, especially through maize and groundnuts, is common in much of Africa and Asia--areas where childhood stunting and underweight are also common, due to a variety of possibly interacting factors such as enteric diseases, socioeconomic status, and suboptimal nutrition. The effects of aflatoxin on growth impairment in animals and human children are reviewed, including studies that assess aflatoxin exposure in utero and through breastfeeding. Childhood weaning diets in various regions of the world are briefly discussed. This review suggests that aflatoxin exposure and its association with growth impairment in children could contribute a significant public health burden in less developed countries.

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Aflatoxin exposure in utero causes growth faltering in Gambian infants.

Paul C Turner, Andrew C Collinson, Yin Cheung … (2007)

Growth faltering in West African children has previously been associated with dietary exposure to aflatoxins, particularly upon weaning. However, in animal studies in utero exposure to low levels of aflatoxin also results in growth faltering.

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Linear growth deficit continues to accumulate beyond the first 1000 days in low- and middle-income countries: global evidence from 51 national surveys.

Edward A. Frongillo, Piet L. J. M. Leroy, Marie Ruel … (2014)

Growth faltering is usually assessed using height-for-age Z-scores (HAZs), which have been used for comparisons of children of different age and sex composition across populations. Because the SD (denominator) for calculating HAZ increases with age, the usefulness of HAZs to assess changes in height over time (across ages) is uncertain. We posited that population-level changes in height as populations age should be assessed using absolute height-for-age differences (HADs) and not HAZs. We used data from 51 nationwide surveys from low- and middle-income countries and graphed mean HAZs and HADs by age. We also calculated annual changes in HAZs and HADs and percentage of total height deficit accumulated annually from birth to age 60 mo using both approaches. Mean HAZ started at -0.4 Z-scores and dropped dramatically up to 24 mo, after which it stabilized and had no additional deterioration. Mean HAD started at -0.8 cm, with the most pronounced faltering occurring between 6 and 18 mo, similar to HAZ. However, in sharp contrast to HAZ, HAD curves had continued increases in the deficit of linear growth from 18 to 60 mo, with no indication of a leveling off. Globally, 70% of the absolute deficit accumulated in height (HAD) at 60 mo was found to be due to faltering during the first "1000 days" (conception to 24 mo), but 30% was due to continued increases in deficit from age 2 to 5 y. The use of HAZ masks these changes because of age-related changes in SD. Therefore, HAD, rather than HAZ, should be used to describe and compare changes in height as children age because detecting any deficit compared with expected changes in height as children grow is important and only HAD does this accurately at all ages. Our findings support the current global programmatic momentum to focus on the first 1000 d. Research is needed to better understand the dynamics and timing of linear growth faltering using indices and indicators that accurately reflect changes over ages and to identify cost-effective ways to prevent growth faltering and its consequences throughout the lifecycle. © 2014 American Society for Nutrition.