Microwaves, a type of nonionizing radiation, may cause harm by denaturing protective enzymes (e.g., glutathione peroxidase), by oxidizing protein thiol groups (causing protein aggregation), or by damaging lens cells via thermoelastic expansion. The protein coagulation caused by electric and heat injuries whitens the lens. This same process is what makes the clear albumen of an egg become white and opaque during cooking. Genetics
The genetic component is strong in the development of cataracts, most commonly through mechanisms that protect and maintain the lens. The presence of cataracts in childhood or early life can occasionally be due to a particular syndrome. Examples of  chromosome abnormalities associated with cataracts include 1q21.1 deletion syndrome, cri-du-chat syndrome, Down syndrome, Pataus syndrome, trisomy 18 (Edwards syndrome), and Turners syndrome, and in the case of neurofibromatosis type 2, juvenile cataract on one or both sides may be noted. Examples of single-gene disorder include Alports syndrome, Conradis syndrome, cerebrotendineous xanthomatosis, myotonic dystrophy, and oculocerebrorenal syndrome or Lowe syndrome. Skin diseases
The skin and the lens have the same embryological origin and so can be affected by similar diseases. Those with atopic dermatitis and eczema occasionally develop shield ulcer cataracts. Ichthyosis is an autosomal recessive disorder associated with cuneiform cataracts and nuclear sclerosis. Basal-cell nevus and pemphigus have similar associations. Smoking and alcohol
Cigarette smoking has been shown to double the rate of nuclear sclerotic cataracts and triple the rate of posterior subcapsular cataracts. Evidence is conflicting over the effect of alcohol.
In immunology, the Arthus reaction () is a type of local type III hypersensitivity reaction. Type III hypersensitivity reactions are immune complex-mediated, and involve the deposition of antigen/antibody complexes mainly in the vascular walls, serosa (pleura, pericardium, synovium), and glomeruli. This reaction is usually encountered in experimental settings following the injection of antigens. History
The Arthus reaction was discovered by Nicolas Maurice Arthus in 1903. Arthus repeatedly injected horse serum subcutaneously into rabbits. After four injections, he found that there was edema and that the serum was absorbed slowly. Further injections eventually led to gangrene. Process
The Arthus reaction involves the in situ formation of antigen/antibody complexes after the intradermal injection of an antigen. If the animal/patient was previously sensitized (has circulating antibody), an Arthus reaction occurs. Typical of most mechanisms of the type III hypersensitivity, Arthus manifests as local vasculitis due to deposition of IgG-based immune complexes in dermal blood vessels. Activation of complement primarily results in cleavage of soluble complement proteins forming C5a and C3a, which activate recruitment of PMNs and local mast cell degranulation (requiring the binding of the immune complex onto FcγRIII), resulting in an inflammatory response. Further aggregation of immune complex-related processes induce a local fibrinoid necrosis with ischemia-aggravating thrombosis in the tissue vessel walls. The end result is a localized area of redness and induration that typically lasts a day or so. Arthus reactions have been infrequently reported after vaccinations containing diphtheria and tetanus toxoid.