The material below is from the NIDCD, which is part of the National Institutes of Health. It's the National Institute on Deafness and Other Communication Disorders.

Smoking cigarettes and loss of smell have been famously linked for many years. Cigarette smoke contains very tiny - ultratrace - amounts of cadmium. You'll note 'cadmium' in the material below.

Drinking alcohol affects smell, also. At least a part of the reason is that metabolizing alcohol requires zinc. And zinc has a connection to an ability to smell; it's not the whole answer, but a significant part.

*******************************

Statistics on Smell [NIDCD Health Information]

Statistics 1-2% of the North American population below the age of 65 years experience smell loss to a significant degree.

According to estimates based on reported research, 1-2% of the North American population below the age of 65 years experience smell loss to a significant degree.

Smell loss is much greater in older populations, with nearly half of individuals between the ages of 65 to 80 years seemingly experiencing some loss of the ability to smell, and nearly three-quarters of those over the age of 80 years experiencing such loss.

Note: These are the best estimates available from studies using actual smell tests. Surveys asking about smell ability without the administration of tests are likely to underestimate smell loss,since many individuals are note aware of their dysfunction unless it is marked. This phenomenon has been noted not only in "normal" populations, but in individuals diagnosed with disorders associated with smell disorders such as Alzheimer's disease and idiopathic Parkinson's disease.

Summary Report
The vast majority of patients presenting to physicians with chemosensory (smell and taste) disturbances, including "taste disturbances," exhibit olfactory dysfunction. As with the case of the taste system, the olfactory system plays a significant role in eating, as most food and beverage flavors are, in fact, dependent upon this system.

Such common "tastes" as chocolate, coffee, strawberry, apple, peach, pizza, steak sauce, and chicken actually reflect olfactory-mediated sensations that require the integrity of CN I. Molecules are released and propelled upwards towards the olfactory receptors via the nasal pharynx during mastication and deglutition (Burdach & Doty, 1987).

The olfactory receptors, unlike the receptors of most sensory systems, are directly exposed to the outside environment, save their protection by a thin layer of mucus, making them relatively susceptible to damage from such exogenous agents as viruses, bacteria, pollutants, and airborne toxins.

Moreover, since the axons of the olfactory receptor cells extend through the foramina of the cribriform plate to synapse within the olfactory bulb of the central nervous system (CNS), they are extremely vulnerable to shearing and tearing from movement of the brain relative to the cranium.

This occurs, for example, in accelerative/decelerative head trauma injuries, even in the absence of fractures, contusions or other objective evidence of trauma (Doty et al., 1997b).

The direct route of the olfactory receptor cells from the nasal cavity to the brain makes the olfactory receptors a major conduit for the movement of environmental agents into the brain, in effect bypassing elements of the blood brain barrier. Among agents known to use this route as a means of entrance into the CNS are such viruses as polio virus (e.g., Bodian & Howe, 1940), rabies virus (e.g., Dean et al., 1963), Herpes simplex virus (e.g., Dinn, 1980), and human immunodeficiency virus (e.g., Brody et al., 1991).

In light of the olfactory anatomy, it is perhaps not surprising the most common causes of permanent smell loss are (a) upper respiratory infections, such as the common cold, (b) head trauma or rapid head acceleration or deceleration, and (c) rhinosinusitis.

Although the data are limited, these three causes do account for the majority of patients who present to physicians with chemosensory disturbance (Duncan & Seiden, 1995). The percent of patients presenting to specialized centers with these etiologies vary slightly from institution to institution, depending upon their referral bases or referral criteria.

In general, about a quarter of patients in such populations have smell loss secondary to URI's, about 20% secondary to head trauma, and 15% secondary to rhinosinusitis (Deems et al., 1991).

Other less common causes of smell loss include chronic alcoholism (Shear et al., 1992), epilepsy Kohler et al., 2001), Kallmann's syndrome (Hudson et al., 1994), Korsakoff's psychosis (Mair et al., pseudohypoparathyroidism (Doty et al., 1997a) and a number of common neurological disorders, including multiple sclerosis (Doty et al., 1997b, 1999), schizophrenia (Moberg et al., 1999), Huntington's disease (Blysma et al., 1998; Moberg & Doty, 1997), Alzheimer's disease (Doty et al., 1987; Murphy et al., 1999), and idiopathic Parkinsonism (Doty et al., 1988).

In the case of multiple sclerosis, the smell dysfunction is directly related to the number of plaques within the subtemporal and orbitofrontal cortices, waxing and waning in relation to plaque activity (Doty et al., 1997, 1999).

In the case of AD and PD, smell loss appears to be the first clinical sign of the disorder, occurring long before the cardinal signs of the syndromes.

In the case of PD, smell loss is unrelated to anti-parkinson medication use and is more common (~ 90%) than tremor (~85%) (Doty et al., 1992).

Smell testing can aid in differential diagnosis, since some neurological diseases, often misdiagnosed as Alzheimer's disease or idiopathic Parkinson's disease, are unaccompanied by meaningful olfactory loss (e.g., major affective disorder (McCaffrey et al., 2000), progressive supranuclear palsy (Doty et al., 1993), essential tremor (Busenbark et al., 1992) and MPTP-induced parkinsonism (Doty et al., 1992).

It is important to note that smell testing of patients at risk for AD may be the best predictor of who later will be clinically diagnosed with AD (Murphy et al., 1988). For example, in an epidemiological study of 1,604 non-demented community-dwelling senior citizens 65 years of age or older, scores on a 12-item odor identification test were a better predictor than scores on a global neuropsychological test of cognitive decline over a subsequent 2-year time period (Graves et al., 1999).

Persons who were anosmic and possessed at least one APOE-4 allele had 4.9 times the risk of having cognitive decline than normosmic persons not possessing this allele (i.e., an odds ratio of 4.9). This is in contrast to the 1.23 times greater risk for cognitive decline in normosmic individuals possessing at least one such APOE allele.

When the data were stratified by sex, women who were anosmic and possessed at least one APOE-4 allele had an odds ratio of 9.71, compared to an odds ratio of 1.90 for women who were normosmic and possessed at least one allele. The corresponding odds ratios for men were 3.18 and 0.67, respectively.

Exposure to a number of toxic agents can induce smell loss. Olfactory loss can occur as a result of exposure to toxins in general air pollution and in workplace settings. In addition to directly damaging the olfactory neuroepithelium, some toxins may produce damage indirectly by inducing upper-respiratory inflammatory responses or infections that, in turn, induce such damage.

The best scientific documentation of toxic exposure in humans is for acrylates, methacrylates, and cadmium, with the former being typically being reversible after removal from the workplace and the latter inducing, in unregulated settings, longer-lasting or permanent effects.

Schwartz et al. (1989) tested the olfactory function of 731 workers at a chemical plant that manufactured acrylates and methacrylates. A nested case-control study designed to assess the cummulative effects of exposure on olfactory function found crude exposure odds ratios (95% confidence intervals) of 2.0 (1.1, 3.8) for all workers and 6.0 (1.7, 21.5) for workers who had never smoked cigarettes. Logistic regression analysis, adjusting for multiple confounders, found exposure odds ratos of 2.8 (1.1, 7.0) and 13.5 (2.1, 87.6) in these same respectives groups and a dose-response relationship between the olfactory and cumulative exposure scores.

Decreased odds ratios were associated with increasing duration since last exposure to the chemicals, implying some degree of reversibility. This seems less likely for cadmium, although similarly sophisticated studies have not been performed.

Yin-Zeng et al. (1985) reported that 28% of individuals who had worked five years or more in a cadmium-refining plant claimed having anosmia, although quantitative testing was not performed. The average concentration of airborne cadmium was said to be relatively low (between 0.004 and 0.187 mg/m3), but still slightly above the current OSHA permissible exposure limit of 0.005 mg/m3).

Rose et al. (1992) found moderate to severe hyposmia, but not anosmia, to n-butanol in 55 workers exposed for an average of 12 years to cadmium fumes, a phenomenon correlated with body burden of cadmium, as measured by urinalysis. Rydzewski et al. (1998) compared the olfactory thresholds of 73 workers involved in the production of cadmium-nickel batteries to that of 43 nonexposed, age- and smoking-matched controls.