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The nineteenth-century phrase “impure air” mixed several different mechanisms. Irritant smoke and dust can damage the respiratory system; toxic gases can poison without causing an infection; crowded, poorly ventilated rooms can increase exposure to infectious material. The historical miasma theory treated foul emanations much more broadly as generators of disease. In particular, the smell of sewage does not itself establish the cause of typhoid fever, cholera or malaria.

For the first part, important real consequences include the following:

For the second part, ordinary outdoor air already contains nitrogen, oxygen, a small amount of carbon dioxide, and variable water vapour. Their presence alone is not evidence of pollution. In a smoky industrial town, soot, mineral dust, products of fuel combustion and sulfur dioxide would be particularly relevant. In occupied rooms, expired carbon dioxide, water vapour and suspended biological material increase unless removed. Decomposing wastes may contribute Ammonia, hydrogen sulfide and other volatile products. The actual mixture depends on sources, ventilation and weather.

For the third part, begin with a defined sampling site and time, record occupancy or industrial activity, and compare with a suitable reference. A volume of air, not simply an unrecorded sniff or a discoloured paper, is the basis of quantitative comparison. Methods available by 1867 include:

The chemical equations underlying two of these qualitative tests areHere the precipitates are barium carbonate and lead sulfide. For the baryta absorption method, in an ideal, fully captured sample with no interfering acid gases, the difference between blank and sample acid requirements satisfieswhere $c_{{\mathrm{H}}^{+}}$ is the amount concentration of titratable acid equivalents and the volumes refer to titration of the entire corresponding absorbent portions; any aliquot requires its scale factor. The factor two follows from the two acid equivalents neutralized per mole of barium hydroxide. This calculation assumes that the barium carbonate precipitate is excluded from the residual-base determination; dissolving it again with the titrant would invalidate the inference.

Odour, visible smoke and room stuffiness are useful prompts to investigate, but no single smell, carbon dioxide value, microscopic field or chemical colour test establishes that air is free of harmful impurities. Specify which material was measured and which uncertainty remains.

The chief physiological routes are abrupt failure of blood circulation, failure of pulmonary ventilation or gas exchange, or catastrophic failure of the central control of those functions. Historical clinical accounts used labels such as syncope, asphyxia and medical coma in explaining deaths; these terms describe broad physiological failures rather than identifying the underlying diseases.^[ref] A brief faint or ordinary medical coma is not itself necessarily fatal.

In primary circulatory failure, effective delivery of blood to the brain stops. Modern examples include ventricular fibrillation, pulseless ventricular tachycardia, severe bradyarrhythmia and asystole. They may arise in coronary artery disease, after myocardial infarction, in cardiomyopathy, or from inherited cardiac ion channel disorders. An electrical cause may leave little distinctive gross evidence at autopsy. These modern mechanisms refine the broad historical description of cardiac syncope.^[ref]

Mechanical interruption of blood circulation gives another group: massive haemorrhage, rupture of an aortic aneurysm, cardiac tamponade, and large pulmonary embolism. The immediate deficit differs in each. Haemorrhage removes circulating volume; cardiac tamponade prevents adequate filling; pulmonary embolism obstructs flow through the pulmonary circulation. All can end with critically low cardiac output even if some electrical activity persists.^[ref]

Respiratory failure includes obstruction of the airway by a foreign body, laryngeal oedema or aspiration; drowning; and depression of breathing by drugs or major brainstem injury. Oxygen delivery then fails and secondary cardiac arrest follows. Carbon monoxide poisoning and cyanide poisoning illustrate related failure of oxygen transport or use: not every hypoxic death is caused by physical obstruction of an airway.^{[ref][ref][ref]}

A major intracranial haemorrhage or rapidly developing brain herniation can destroy or compress the pathways maintaining consciousness and breathing. A severe disturbance of electrolytes, especially potassium, may instead act directly on the heart's electrical function. A fatal seizure can involve respiratory and circulatory mechanisms; sudden unexpected death in epilepsy remains a diagnosis requiring exclusion of other causes, not merely recognition of a history of epilepsy.^[ref]

The practical distinction is between mode, immediate mechanism and underlying cause. For example, rupture of an aneurysm can cause haemorrhage, then circulatory failure, then irreversible hypoxic-ischaemic brain injury. A complete explanation identifies that chain. Inspection, histology, examination of the airway and heart, and appropriately interpreted toxicology may establish it; an unexplained sudden death cannot be assigned a precise cause from its suddenness alone.