If Zika is the cause of microcephaly in Brazil, there should be a sharp spike in the microcephaly rate in Colombia, starting in August, 2016.

If I were in the public arena, I would consider where things will go if Colombia does not spike.

There is a pesticide (pyriproxyfen) that has a reasonable expectation of having a side effect of action like Accutane, the acne drug that caused the epidemic of microcephaly in the early 1980s.

That side effect is action on the retinoic acid receptor, like pyriproxyfen's insect juvenile hormone agonist cousin (methoprene) does.

Pyriproxyfen was put into the water and piped into potable supplies where the microcephaly is also found.

Some Brazilian and Argentine (Medardo Avila Vazquez) M.D.s have already suggested that pyriproxyfen, and not Zika is the cause, and I have suggested this mechanism to them.

Their hypothesis has been shelved by the experts, but experts are often intrenched in a narrow view.

If Colombia does not blow up with microcephaly, the pesticide is back on the table in a big way.

Plausibility and opportunity (exposure) are in place, and there is no reasonable alternate explanation for the outbreak of microcephaly.

Be alert.

A paper published in August 2016 supports the contention that the insecticide (pyriproxyfen) put into the drinking water where most of the microcephaly happened, can cause developmental defects in vertebrates.

Environ Pollut. 2016 Sep 1. pii: S0269-7491(16)30979-4. doi: 10.1016/j.envpol.2016.08.061. [Epub ahead of print]

Assessment of the developmental and neurotoxicity of the mosquito control larvicide, pyriproxyfen, using embryonic zebrafish.

Truong L(1), Gonnerman G(2), Simonich MT(3), Tanguay RL(4).

Author information:

(1)Department of Environmental and Molecular Toxicology, The Sinnhuber Aquatic Research Laboratory, and the Environmental Health Sciences Center at Oregon State University, Corvallis, OR, USA. Electronic address: Lisa.truong@oregonstate.edu.

(2)Department of Environmental and Molecular Toxicology, The Sinnhuber Aquatic Research Laboratory, and the Environmental Health Sciences Center at Oregon State University, Corvallis, OR, USA. Electronic address: Gman@oregonstate.edu.

(3)Department of Environmental and Molecular Toxicology, The Sinnhuber Aquatic Research Laboratory, and the Environmental Health Sciences Center at Oregon State University, Corvallis, OR, USA. Electronic address: mtsimonich@oregonstate.edu.

(4)Department of Environmental and Molecular Toxicology, The Sinnhuber Aquatic Research Laboratory, and the Environmental Health Sciences Center at Oregon State University, Corvallis, OR, USA. Electronic address: Robert.tanguay@oregonstate.edu.

In 2014, as an attempt to address the Zika health crisis by controlling the mosquito population, Brazil took the unprecedented action of applying a chemical larvicide, pyriproxyfen, to drinking water sources. The World Health Organization has established an acceptable daily intake of pyriproxyfen to be 100 ug per kg of body weight per day, but studies have demonstrated that at elevated doses (>5000 mg/kg), there are adverse effects in mice, rats and dogs. To better understand the potential developmental toxicity of pyriproxyfen, we utilized the embryonic zebrafish. Our results demonstrate that the concentration resulting in 50% of animals presenting adverse morphological effects (EC50), including craniofacial defects, was 5.2 uM for daily renewal exposure, and above this concentration, adverse behavioral effects were also observed in animals that followed a static exposure regimen. Thus, zebrafish data suggest that the developmental toxicity of pyriproxyfen may not be limited to insects.

Copyright 2016 Elsevier Ltd. All rights reserved.

DOI: 10.1016/j.envpol.2016.08.061

PMID: 27593350 [PubMed - as supplied by publisher]

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