Environmental Engineering Reference
In-Depth Information
in metabolism, homeostasis, thermoregulation, and hormonal regulation. Next to the
digestive tract, the skin is populated by the largest number of immune cells and plays a
pivotal role in innate and adaptive immune response.
16.2 Problems with Terminology
Considering the above-mentioned complexity and importance of the skin functions,
one can wonder why some people consider the skin to be merely a kind of “encasing”
for the internal organs. Specifically, it is impossible to defend some toxicologists' views
on the skin as a kind of semipermeable membrane through which pesticides enter the
body. This idea is reflected in the popular misnomer “dermal toxicity” that has been
used through decades for internal or systemic toxicity of pesticides absorbed via the
skin (Noakes and Sanderson 1969; Zendzian 2003). The logics would dictate that the
term should be used in reference to toxic damage caused by pesticides to the skin itself,
in analogy to, for example, “hepatotoxicity,” “cardiotoxicity,” or “neurotoxicity” (mean-
ing toxicity to the respective organs, rather than toxicity of the agents absorbed through
the liver, heart, or nerves). In order to avoid further confusion, the misleading term
“dermal toxicity” should be ultimately and definitely abandoned. In accordance with
scientific clarity, the toxic effects of dermally absorbed pesticides to the internal organs
could be referred to as “percutaneous toxicity” (Whitesell et al. 1947), “toxicity of der-
mally absorbed pesticides” (Latuszynska et al. 1999), or perhaps “transdermal toxicity.”
The word “dermatotoxicity” (Kimura et al. 1998; Kataranovski et al. 2005) should be
instead promoted as the actual term for describing skin damage caused by chemical
substances, also when ingested, inhaled, or administered parenterally (Ali and Oehme
1992; Muhammad et al. 2010).
16.3 Effects of Pesticides in the Skin
Pesticides may act upon the skin as irritants, sensitizing haptens, photohaptens, and car-
cinogens. They may also possess pharmacological properties that can alter the physio-
logical functions of the skin. The underlying mechanisms are only partially known, and
in most cases, we have to retreat to the general understating of the skin effects caused
by xenobiotics, rather than specific data from studies on specific pesticides. The reader is
directed elsewhere for an overview of the general mechanisms underlying irritant and
allergic contact dermatitis (ACD) (English 2004; Gober and Gaspari 2008; Nosbaum et al.
2009), photosensitivity (Lankerani and Baron 2004; Kerr and Ferguson 2010), chemically
induced porphyrias (Downey 1999), and carcinogenesis (Bowden et al. 1993; Slaga et al.
1995). Only research specifically devoted to studying the responses to pesticide within
the skin will be discussed further in this paragraph. At present, information on this
topic is scarce and limited to a few pesticides only. As many other xenobiotics, pesticides
may act as sensitizing haptens or autoimmunogenic compounds that trigger pathologic
reactions via thymus-dependent mechanisms. One of the pesticides that causes adverse
immune effects in both man and rat in the T cell-dependent manner is hexachlorobenzene
 
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