Efectos toxicológicos del uso prolongado e intenso de emisiones de espirales contra mosquitos en ratas y sus implicaciones sobre el control de la malaria

Abstract

Efectos toxicológicos del uso prolongado e intenso de emisiones de espirales contra mosquitos en ratas y sus implicaciones sobre el control de la malaria. Mosquito coil is a vector control option used to prevent malaria in low income counties, while some studies have addressed this issue, additional reseach is required to increase knowledge on the adverse health effects caused by the prolonged use of coils. In this study we investigated the toxicological effects of fumes from two locally manufactured mosquito coil insecticides (with pyrethroids: transfluthrin and d-allethrin as active ingredients) on male albino rats. For this, we recorded the haematological and biochemical indices, and made histopathology and mutagenicity evaluations in rats exposed to mosquito fumes during 2, 4, 8, 12 and 16 week periods. Haematological determination was performed using automated hematology analyzer to determine White Blood Cell (WBC), Packed Cell volume (PCv), Red Blood Cell (RBC) and Platelet (PLT) counts, while biochemical evaluations were determined using available commercial kits. Gross histopathological changes were studied for the kidney, liver and lungs in sacrificed rats. The rat sperm head abnormalities assessment was used to evaluate mutagenicity. Mosquito coil fumes produced significant increase (P<0.05) in the levels of total protein, total albumin and bilirubin, when animals were exposed from two weeks to 16 weeks with transfluthrin. Similarly, elevation in the activities of aspartate amino transferase, alanine amino transferase and alanine phosphatase, increased significantly in both insecticides. Increase in WBC, RBC and PCv were recorded for all the exposure periods, however PLT count showed no significant increase (P>0.05). Mutagenicity assessment revealed sperm abnormality was statistically significant (P<0.05) compared with the control at 8, 12 and 16 weeks post exposure to transfluthrin. Histological studies revealed severe lung damage evidenced by interstitial accumulations, pulmonary oedema and emphysema in exposed rats. Intracellular accumulations and severe sinusoidal congestion of liver cells were observed from 12 weeks exposure, indicating liver damage. Our studies indicate that mosquito coil fumes do initiate gradual damage to the host. These pathological effects must be taken into consideration by the malaria control program, particularly when regulating their long term and indoor usage. Rev.

Toxicological and histopathological alterations in the heart of young and adult albino rats exposed to mosquito coil smoke.

“…Moreover, obtained data also showed signi cant increase in serum EPO hormone in both exposed groups. Idowu et al (2013) suggested that the increase in EPO hormone is responsible for stimulating bone marrow to produce RBCs to overcome hypoxia. In turn, the maintenance of normal levels of hematological parameters in the present study can be attributed to the increase of EPO hormone in the exposed groups.…”

Toxicological and histopathological alterations in the heart of young and adult albino rats exposed to mosquito coil smoke

“…Moreover, obtained data also showed significant increase in serum EPO hormone in both exposed groups. Idowu et al ( 2013 ) suggested that the increase in EPO hormone is responsible for stimulating bone marrow to produce RBCs to overcome hypoxia. In turn, the maintenance of normal levels of hematological parameters in the present study can be attributed to the increase of EPO hormone in the exposed groups.…”

The Teratogenic Effect of Dimefluthrin-Based Mosquito Coils on Pregnant Mice (Mus musculus L.)

“…Research has shown that the use of pyrethrin-based mosquito coils can significantly increase the number of leukocytes, particularly basophils and lymphocytes (Garba et al, 2007;Al-Mamun et al, 2017). Long-term exposure to pyrethroids can also affect the biochemical parameters of blood (Narendra et al, 2007;Idowu et al, 2013), increase the levels of reactive oxygen species (ROS), and lead to over-expression of the gene p53, which is considered the first stage of cellular apoptosis mediated by mitochondria (Madhubabu & Yenugu, 2012).…”