They exist primarily in sandy or loamy soil and cannot live in clay or muck. Rainfall averages must be more than 1,000 mm (39 in) a year for them to survive. Only if these conditions exist can the eggs hatch. Infective larvae of N. americanus can survive at higher temperatures, whereas those of A. duodenale are better adapted to cooler climates. Generally, they live for only a few weeks at most under natural conditions, and die almost immediately on exposure to direct sunlight or desiccation.Infection of the host is by the larvae, not the eggs. While A. duodenale can be ingested, the usual method of infection is through the skin; this is commonly caused by walking barefoot through areas contaminated with fecal matter. The larvae are able to penetrate the skin of the foot, and once inside the body, they migrate through the vascular system to the lungs, and from there up the trachea, and are swallowed. They then pass down the esophagus and enter the digestive system, finishing their journey in the intestine, where the larvae mature into adult worms.Once in the host gut, Necator tends to cause a prolonged infection, generally 1 to 5 years (many worms die within a year or two of infecting), though some adult worms have been recorded to live for 15 years or more. Ancylostoma adults are short-lived, surviving on average for only about 6 months.
Toxic oil syndrome 
(TOS) or simply toxic syndrome (Spanish: síndrome del aceite tóxico or síndrome tóxico) is a musculoskeletal disease. A 1981 outbreak in Spain which affected about 20,000 people, with over 300 dying within a few months and a few thousand remaining disabled, is thought to have been caused by contaminated colza (rapeseed) oil. It was unique because of its size, the novelty of the clinical condition, and the complexity of its aetiology. Its first appearance was as a lung disease, with unusual features, though the symptoms initially resembled a lung infection. The disease appeared to be restricted to certain geographical localities, and several members of a family could be affected, even while their neighbours had no symptoms. Following the acute phase, a range of other chronic symptoms was apparent. Alternative mechanisms
The conclusion of the Joint WHO/CISAT Scientific Committee for the Toxic Oil Syndrome from 2002, that oil was the cause for TOS, is based only on epidemiological evidence, since up to now, experimental studies performed in a variety of laboratory animals have failed to reproduce the symptoms of human TOS. None of the in vivo or in vitro studies performed with toxic-oil-specific components, such as fatty acid anilides, and esters of 3-(N-phenylamino)-1,2-propanediol (abbreviated as PAP), have provided evidence that these markers are causally involved in the pathogenesis of TOS.Specifically, three possible causative agents of TOS are PAP (3-(N-phenylamino)-1,2-propanediol), the 1,2-dioleoyl ester of PAP (abbreviated OOPAP), and the 3-oleoyl ester of PAP (abbreviated OPAP).