RESUMO
Children living near artisanal and small-scale gold mining (ASGM) are at risk of exposure to mercury, a neurotoxicant. It is not certain whether such exposures are harming development, as they occur in underresourced contexts entwined with other stressors, such as malnutrition and enteric infection. This study sought to investigate the association between hair-mercury levels and visual-motor, cognitive, and physical development among children living near ASGM in the Peruvian Amazon. Total hair-mercury levels were measured in 164 children ages 5-12 living in Madre de Dios, Peru. Primary outcomes included Visual-Motor Integration assessed via the Beery-VMI Developmental Test, General Cognitive Ability assessed via the Batería-III Woodcock-Munoz (Spanish-language Woodcock-Johnson Tests of Cognitive Abilities), and Physical Health assessed via anthropometry/hemoglobin counts. Mean (SD) hair-mercury level was 2.06 (2.43) µg/g. Fifty-four children (32.9%) had hair-mercury levels above the World Health Organization reference level of 2.0 µg/g. After controlling for sex, child age, maternal education, and family socioeconomic status, each one unit increase in log hair-mercury level was associated with a 1.01 unit decrease in Visual-Motor Integration (95%CI: -2.06, 0.05, p = 0.061), a 2.59 unit decrease in General Cognitive Ability (95%CI: -4.52, -0.66, p = 0.012), and a 2.43 unit decrease in Physical Health (95%CI: -5.34, 0.49, p = 0.096). After adjustment for covariates, children with hair-mercury levels exceeding the World Health Organization reference level scored 4.68 IQ points lower in Cognitive Ability than their peers. Mercury exposures related to ASGM may be harming child development in the Peruvian Amazon. Children in this region may benefit from intervention to reach their full developmental potential.
RESUMO
Mucosal leishmaniasis (ML) is associated with progressive tissue destruction and granuloma formation, often after a considerable period of latency from an initial cutaneous infection. We report a case of recurrent epistaxis of 3 years duration and nasopharyngeal obstruction in a woman with treated cutaneous leishmaniasis nearly 30 years before and with no further exposure to Leishmania. Computed tomography revealed nasal septal perforation and histopathology demonstrated chronic inflammation. Microscopy was negative for amastigotes, but molecular testing of nasal mucosa biopsy detected Leishmania (Viannia) braziliensis. The patient underwent 28 days of treatment with IV sodium stibogluconate and her symptoms improved significantly. Sixteen months after treatment, she continues to have episodic epistaxis and detectable parasite load in her nasal lesion. Although ML is known to take years to decades to develop, there are few reported cases in the literature of such a long latency period. This report highlights the importance of considering ML in the differential diagnosis of chronic epistaxis in countries where leishmaniasis is endemic or in immigrants from these countries, even when presentation occurs decades after leaving an endemic region.